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S Mokmeli MD, M Vetrici MD. Low level laser therapy as a modality to attenuate cytokine storm at multiple levels, enhance recovery, and reduce the use of ventilators in COVID-19. Can J Respir Ther 2020;56:1-7. doi: 10.29390/cjrt-2019-015. The global pandemic COVID-19 is a contagious disease and its mortality rates ranging from 1% to 5% are likely due to acute respiratory distress syndrome (ARDS), and cytokine storm. A significant proportion of patients who require intubation succumb to the disease, despite the availability of ventilators and the best treatment practices. Researchers worldwide are in search of anti-inflammatory medicines in the hope of finding a cure for COVID-19. Low-level laser therapy (LLLT) has strong, anti-inflammatory effects confirmed by meta-analyses, and it may be therapeutic to ARDS. LLLT has been used for pain management, wound healing, and other health conditions by physicians, physiotherapists, and nurses worldwide for decades. In addition, it has been used in veterinary medicine for respiratory tract disease such as pneumonia. Laser light with low-power intensity is applied to the surface of the skin to produce local and systemic effects. Based on the clinical experience, peer-reviewed studies, and solid laboratory data in experimental animal models, LLLT attenuates cytokine storm at multiple levels and reduces the major inflammatory metabolites. LLLT is a safe, effective, low-cost modality without any side-effects that may be combined with conventional treatment of ARDS. We summarize the effects of LLLT on pulmonary inflammation and we provide a protocol for augmenting medical treatment in COVID-19 patients. LLLT combined with conventional medical therapy has the potential to prevent the progression of COVID-19, minimize the length of time needed on a ventilator, enhance the healing process, and shorten recovery time.
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RESEARCH ARTICLE
Low level laser therapy as a modality to attenuate cytokine
storm at multiple levels, enhance recovery, and reduce
the use of ventilators in COVID-19
Soheila Mokmeli MD Anesthesiologist1, Mariana Vetrici MD, PhD2
S Mokmeli MD, M Vetrici. Low level laser therapy as a modality to attenuate cytokine storm at multiple levels, enhance recovery, and reduce
the use of ventilators in COVID-19. Can J Respir Ther 2020;56:1–7. doi: 10.29390/cjrt-2019-015.
The global pandemic COVID-19 is a contagious disease and its mortality rates ranging from 1% to 5% are likely due to acute respiratory distress syndrome
(ARDS), and cytokine storm. A significant proportion of patients who require intubation succumb to the disease, despite the availability of ventilators and
the best treatment practices. Researchers worldwide are in search of anti-inflammatory medicines in the hope of finding a cure for COVID-19. Low-level
laser therapy (LLLT) has strong, anti-inflammatory effects confirmed by meta-analyses, and it may be therapeutic to ARDS. LLLT has been used for pain
management, wound healing, and other health conditions by physicians, physiotherapists, and nurses worldwide for decades. In addition, it has been used
in veterinary medicine for respiratory tract disease such as pneumonia. Laser light with low-power intensity is applied to the surface of the skin to produce
local and systemic effects. Based on the clinical experience, peer-reviewed studies, and solid laboratory data in experimental animal models, LLLT attenu-
ates cytokine storm at multiple levels and reduces the major inflammatory metabolites. LLLT is a safe, effective, low-cost modality without any side-effects
that may be combined with conventional treatment of ARDS. We summarize the effects of LLLT on pulmonary inflammation and we provide a protocol
for augmenting medical treatment in COVID-19 patients. LLLT combined with conventional medical therapy has the potential to prevent the progression
of COVID-19, minimize the length of time needed on a ventilator, enhance the healing process, and shorten recovery time.
Key Words: COVID-19; ARDS; cytokine storm; low level laser therapy; anti-inflammator y; ventilator; photobiomodulation
INTRODUCTION
What is low level laser therapy?
Low level laser therapy (LLLT) is also known as cold laser therapy or photo-
biomodulation therapy. LLLT utilizes visible light and infrared laser beams
in the range of 450–1000 nm. Single wavelength or monochromatic light is
emitted from a low-intensity laser diode (<500 mW). The light source is
placed in contact with the skin, allowing the photon energy to penetrate
tissue, where it interacts with various intracellular biomolecules to restore
normal cell function and enhance the body’s healing processes [1]. This
contrasts with the thermal effects produced by the high-power lasers that are
used in cosmetic and surgical procedures to destroy tissue [1], as mentioned
in the PubMed Medical Subject Heading (MeSH) subheading for LLLT.
LLLT effects are not due to heat but rather to a photochemical reaction
that occurs when a photoacceptor molecule within the cell absorbs a pho-
ton of light, becomes activated, and changes the cell’s membrane permea-
bility and metabolism. Presently, cytochrome c oxidase, opsins and their
associated calcium channels, and water molecules have been identified as
the main mediators of the photochemical mechanisms [2]. This leads to
increased mRNA synthesis and cell proliferation. LLLT produces reactive
oxygen species (ROS) in normal cells, but ROS levels are lowered when it
is used in oxidatively stressed cells, like in animal models of disease. LLLT
up-regulates antioxidant defenses and decreases oxidative stress [2].
Low-level lasers are a safe, noninvasive technology approved by both
the US Food and Drug Administration and Health Canada for several
chronic and degenerative conditions, temporary pain relief, cellulite
treatment, body contouring, lymphedema reduction, hair growth, and
chronic musculoskeletal injuries. LLLT increases microcirculation, lym-
phatic drainage, and cellular metabolism, thereby relieving many acute
and chronic conditions.
The MeSH database in PubMed contains more than 7000 articles on
LLLT. The effects of LLLT have been confirmed through several meta-
analysis studies and include anti-inflammatory [3] and analgesic effects [4],
tissue healing [5], treating tendinopathy [6], and improving lymphedema
[7]. Recent lab and animal studies suggest LLLT is ready for clinical trials
over myocardial infarction [5]. In 2010, a meta-analysis concluded that there
was strong evidence of an anti-inflammatory effect of LLLT [3].
To date, published reports indicate that LLLT up-regulates antioxi-
dant defenses and decreases ROS in oxidatively stressed cells and animal
models of disease. The anti-inflammatory effect of LLLT directly
addresses the main pathology of disorders such as musculoskeletal,
lungs, wounds, brain, trauma, etc. LLLT reduces NF-kB, a protein com-
plex that controls transcription of DNA, in pathological conditions.
Reports have shown reductions in reactive nitrogen species and prosta-
glandins in various animal models [2].
LLLT has diverse effects [8]:
reduces pain related to inflammation via dose-dependent reduc-
tion of prostaglandin E2, prostaglandin-endoperoxide synthase-2,
IL-1, IL-6, TNFa, as well as the cellular influx of neutrophils, oxi-
dative stress, edema, and bleeding;
1Canadian Optic and Laser Center (Training Institute), Victoria, BC, Canada
2Department of Biological Sciences, University of Lethbridge, Lethbridge, AB T1K 3M4, Canada
Correspondence: Soheila Mokmeli, Canadian Optic and Laser Center (Training Institute), 744A Lindsay Street, Victoria, BC V8Z 3E1, Canada.
Tel.: +1 (250) 480-7868, E-mail: dr.mokmeli@yahoo.com Mariana A. Vetrici, Department of Biological Sciences, University of Lethbridge, 4401 University
Drive, Lethbridge, AB T1K 3M4, Canada, Tel.: +1 (865) 888-3095, E-mail: marianavetrici@gmail.com
Soheila Mokmeli and Mariana Vetrici
2 Can J Respir Ther Vol 56
decreases edema and swelling by increasing lymphatic drainage;
increases collagen and protein production, and cell proliferation;
accelerates wound healing and scar formation;
improves quality and tensile strength of tissue;
stimulates nerve function and regeneration;
accelerates bone regeneration and remineralization;
reduces the pain threshold and enhances endorphins;
washes inflammatory debris away from the injured site; and
augments blood flow.
LLLT has been used in respiratory tract diseases since 1978. Empirical
practice on over 1000 patients produced data pertaining to chronic pneu-
monia, acute pneumonia, asthma, and chronic bronchitis in children,
adults, and elderly. Common findings include reduced chest pain and
heaviness; normalization of respiratory function; improved blood, immu-
nological, and radiological parameters; and shortened recovery times. In
community-acquired pneumonia, intravenous LLLT of blood added to
conventional treatment significantly promoted the bactericidal activity of
neutrophils. In asthma, the addition of LLLT was more effective than
medical treatment alone and it shortened the duration of treatment and
recovered bronchial sensitivity to sympathomimetics [9–11]. In newborns
with pneumonia, LLLT combined with conventional medical regimens
optimized the treatment infectious and inflammatory diseases, reduced
the incidence of complications, and shortened recovery periods [12].
LLLT is a well-known treatment modality in veterinary medicine.
Upper and lower respiratory conditions in dogs and cats are common, and
viral and bacterial infections are often highly contagious. Regardless of
etiology, inflammation is the major pathology of these conditions. The
addition of LLLT to conventional treatment alleviates symptoms and stim-
ulates the healing process in tissues. General guidelines for the use of laser
therapy in animals and protocols for specific conditions are published [13].
The pathogenesis of COVID-19 in respiratory tract
Coronaviruses are a large group of viruses that affect animals. In humans,
they produce diseases such as the common cold, severe acute respiratory
syndrome (SARS) and Middle East respiratory syndrome. The disease
caused by the novel coronavirus, SARS-CoV-2, has been named COVID-
19 and the clinical manifestations range from asymptomatic to severe
acute respiratory distress syndrome (ARDS) to death [14].
Respiratory viruses infect either the upper or lower airways. Typical
upper-respiratory infections are milder, more contagious, and spread eas-
ily, whereas lower-respiratory infections spread much less frequently but
are more severe and dangerous. SARS-CoV-2 appears to infect both
upper and lower airways. It spreads while still limited to the upper air-
ways, before traveling into the deeper respiratory tract and leading to
severe symptoms [15].
SARS-CoV-2 attaches to a protein called angiotensin converting
enzyme (ACE2), on the surface of cells in the respiratory tract. As SARS-
CoV-2 attacks the cells, dead cells flow down and block the airways with
debris while the virus moves deeper into the lungs. Breathing becomes
difficult because the lungs become clogged with dead cells and fluid.
The immune system attacks the virus causing inflammation and fever. In
severe cases, the immune system goes wild, causing more damage to the
lungs than the actual virus. Blood vessels dilate to increase blood flow
and become more permeable to maximize transport of chemical and cel-
lular mediators the infection site. Inevitably, the lungs get filled with
fluid. This exaggerated immune response is called cytokine storm and it
leads to ARDS, fever, multiorgan failure, and death [15, 16].
During cytokine storm, the immune system attacks indiscriminately
without clearing the specific targets. Cytokine storm also affects other
organs, especially if people already have chronic diseases [15]. The sever-
ity of cytokine storm determines who is hospitalized and who will be
treated in the intensive care unit (ICU). The classification of COVID-19
is summarized in Table 1 [17].
The morbidity and mortality of COVID-19 are due to excessive
inflammatory cytokine production and immune hyperactivity. Alveolar
macrophage activation and cytokine storm are the main pathogenesis of
severe COVID-19. The pathological features include exudation and
hemorrhage, epithelial injuries, infiltration of macrophages into the
lungs, and fibrosis of lung tissue. The mucous plug with fibrinous exu-
date in the alveoli and the activation of alveolar macrophage are charac-
teristic abnormalities [18, 19]. Chemical and genetic studies have shown
that the pulmonary endothelium is a key component of the cytokine
storm. Therefore, modulation of the involved cellular signaling pathways
may have therapeutic effects [20, 21].
COVID-19 begins when SARS-CoV-2 uses ACE2 as the entry recep-
tor for infection [22]. This induces ACE2 downregulation and shedding.
Loss of ACE2 from the endothelium causes dysfunction of the renin-an-
giotensin system, and it enhances inflammation and vascular permeabil-
ity. Shedding of ACE2 from the endothelium releases enzymatically
active soluble ACE2 (sACE2), which is tightly linked to tumor necrosis
factor alpha (TNF-α) production in cell culture [23].
Multiple signaling pathways are activated during an immune
response and cytokine storm. The P2X purinoceptor 7 (P2X7r) is major
TABLE 1
The staging and classication of COVID-19 [17]
Class Symptoms Imaging Respiratory criteria
Mild infection Mild Negative signs of pneumonia Normal
Moderate infection Fever and upper respiratory
tract symptoms
Positive signs of pneumonia Normal
Severe infection Fever, upper and lower
respiratory tract symptoms
>50% lesion progression
within 24–48 hours
Respiratory rate ≥ 30 /min
O2 saturation ≤ 93% at rest
Arterial partial pressure of O2 (PaO2)/oxygen concentration (FiO2)
≤ 300 mm Hg
Critical infection Respiratory failure requiring
mechanical ventilator
and (or)
presence of shock
and (or)
other organ failure that requires
monitoring and (or) treatment in
the ICU
> 50% lesion progression
within 24–48 hours
Early stage:
• Oxygenation index 100.1–149.9 mmHg.
• Respiratory system compliance (RSC) ≥ 30 ml/cmH2O.
• No organ failure other than the lungs.
Middle stage:
• 60 mmHg < O2 index ≤ l00 mmHg.
• 30 mL/cmH2O > RSC ≥ 15 mL/cmH2O.
• Maybe complicated by mild or moderate dysfunction of other organs.
Late stage:
• O2 index ≤ 60 mmHg.
• RSC < 15 mL/cmH2O.
Diffuse consolidation of both lungs that requires the use of extracorpo-
real membrane oxygenation or failure of other vital organs.
Note: A conrmed case is based on the epidemiological history (including cluster transmission), clinical symptoms (fever and respiratory symptoms), lung imaging,
and results of SARS-CoV-2 nucleic acid detection and serum-specic antibodies [17].
Low level laser therapy for COVID-19
Can J Respir Ther Vol 56 3
factor involved in activation of the cytokine storm and lung pathology in
response to viruses [24, 25], infection, inflammation, hypoxia, or trauma
[26]. P2X7r is an adenosine triphosphate (ATP) gated, nonselective cat-
ion channel, allowing Ca2+ and Na+ influx and K+ efflux. Extracellular
ATP plays a central role in apoptotic cell death [27], the induction of
inflammation [28], and mitochondrial failure in monocytes [29]. P2X7r
mediates ATP-induced cell death in different cells and it promotes
assembly and release of proinflammatory interleukins (IL -1β and IL-18)
from immune cells after exposure to lipopolysaccharide and ATP [27].
P2X7r is constitutively expressed in many cells, including respiratory epi-
thelial cells and most immune cells like neutrophils, monocytes, macro-
phages, dendritic, natural killer, B and T lymphocytes [27].
Studies stratified COVID-19 patients as: (i) severe symptoms and
ICU admission and (ii) mild and moderate symptoms requiring hospital-
ization but not ICU [17, 19]. The severe patients have significantly
higher levels of plasma pro-inflammatory factors (IL-2, IL-7, IL -10,
GSCF, IP-10, MCP-1, MIP1A, TNF-α) [19] and (IL-2, IL-6, IL-10, TNF-α)
[18] than non-ICU patients, and they were likely in cytokine storm [17,
19]. These findings justify the use of IL-6 receptor antagonists [18, 19];
however, a therapy to reduce inflammation at multiple levels, such as
LLLT, could be more successful in controlling the unbalanced immune
response (Figure 1).
The effects of LLLT on pulmonary inflammation
LLLT is effective against cytokine storm and ARDS while promoting
healing and tissue regeneration. Experimental and animal models of pul-
monary disease and infection have revealed multiple cellular and molec-
ular effects, which are both local and systemic. LLLT reduces
inflammation without impairing lung function in acute lung injuries
and is a promising therapeutic approach for lung inflammatory diseases
such as Chronic obstructive pulmonary disease [26].
In murine models of acute inflammation of the airways and lungs,
transcutaneous LLLT delivered over the trachea decreases pulmonary
microvascular leakage [30, 31], IL-1b levels [26, 30], IL -6 [26, 32],
MIP-2 mRNA expression [30], and intracellular ROS production [24].
LLLT produces anti-inflammator y effects on tracheal hyperactivity, and
reduces neutrophil influx [26, 30, 32–34] by inhibiting COX-2-derived
metabolites [33]. In ARDS, LLLT elevates cyclic adenosine monophos-
phate [32, 34], a signaling molecule that stimulates IL-10 and G-CSF expres-
sion and blocks TNF-a and MIP-1. LLLT also reduces TNF-a levels in
bronchoalveolar lavage fluid and alveolar macrophages [26, 31–34]. In hem-
orrhagic lesions of the lungs, LLLT significantly reduces the hemorrhagic
index and myeloperoxidase activity, to levels comparable to Celecoxib [35].
LLLT contributes to the resolution of inflammation by upregulating
IL-10 and downregulating P2X7r. LLLT changes the profile of inflamma-
tory cytokines and elevates IL-10 [26, 31, 36], known as human cytokine
synthesis inhibitory factor, in the lung and abolishes lung inflammation
via a reduction of inflammatory cytokines and mast cell degranulation
[31]. LLLT decreases collagen deposition as well as the expression of the
P2X7r [26].
LLLT contributes to healing by promoting apoptosis of inflamma-
tory cells while suppressing apoptotic pathways in lung tissue. In a model
of acute lung injury, LLLT reduced DNA fragmentation and apoptotic
pathways via increased B-cell-lymphoma-2 (Bcl-2), the key regulator of the
intrinsic or mitochondrial pathway for apoptosis, in alveolar epithelial
cells while promoting DNA fragmentation in inflammatory cells [37]. In
pulmonary idiopathic fibrosis, LLLT inhibits pro-inflammatory cyto-
kines and increases expression of proliferating cell nuclear antigen [38],
attenuates airway remodeling by balancing pro- and anti-inflammatory
cytokines in lung tissue, and inhibiting fibroblast secretion of the
pro-fibrotic cytokines [36].
LLLT provides synergy in combination with medical treatment. It has
a synergic anti-inflammatory action over alveolar macrophages pretreated
with N-acetyl cysteine, an effective oral medicine for coughs and some lung
conditions [39]. The synergic effects of LLLT combined with conventional
treatments were reported on over 1000 patients in Russian studies [9–11].
FIGURE 1
The effects of SARS-CoV-2 on alveolar cell and cytokine storm.
Soheila Mokmeli and Mariana Vetrici
4 Can J Respir Ther Vol 56
Extended time on ventilators causes lung injury but LLLT minimizes
this side effect. In experimental models of ventilator-induced lung injury
(VILI), LLLT following VILI resulted in lower injury scores, decreased
total cell count and neutrophil count in bronchoalveolar lavage, and
reduced alveolar neutrophil infiltration. LLLT in an experimental model
of VILI in rats demonstrated the anti-inflammatory effect via decreased
lung injury scores and lower counts of neutrophils in alveolar, intersti-
tial, and bronchial lavage [39] (Figure 2).
Evidence from the literature supports the use of LLLT for the treat-
ment of COVID-19.
It has significant anti-inf lammatory effects confirmed by meta-
analyses. Eleven cell studies, 27 animal studies, and another six
animal studies for drug comparisons and LLLT interactions veri-
fied that there is strong evidence of an anti-inflammatory effect of
LLLT. The scale of the anti-inf lammatory effect is not significantly
different than non-steroidal anti-inflammatory drugs, but it is
slightly less than glucocorticoid steroids [3].
It has diverse applications and effects confirmed through several
meta-analysis studies include analgesia [4], tissue healing [5], treat-
ing tendinopathy [6], and improved lymphedema [7].
LLLT is approved by the US FDA and Health Canada for several
chronic and degenerative conditions, temporary pain relief, cellu-
lite treatment, body contouring, lymphedema reduction, and hair
growth. It has been used in veterinary medicine for upper and
lower respiratory conditions in dogs and cats [13].
It has been used for human respiratory tract disease. Empirical use
on over 1000 patients produced data pertaining to chronic pneu-
monia, acute pneumonia, asthma, and chronic bronchitis in chil-
dren, adults, and the elderly [9–12]. Light therapy and LLLT has
been mentioned as a potential treatment for pandemic coronavirus
infections [40].
The anti-inf lammatory effect of LLLT in lung inflammation is con-
firmed in at least 14 experimental animal studies. LLLT attenuates
cytokine storm at multiple levels and reduces the major inflamma-
tory metabolites such as IL-6 and TNF-α. IL-6 antagonists are
being investigated for treating COVID-19 but LLLT reduces the
production of IL-6, as well as other chemokines and metabolites
[26–39, 41].
There are US FDA and Health Canada approved laser machines
for pain management, lymphedema after breast cancer surgery,
and cellulite treatments that can be used and set to treat lung
inflammation.
LLLT is an affordable modality compared with other treatments
and medicines like IL-6 antagonists. LLLT is a safe, effective, low-
cost modality without any reported side-effects compared with
other approaches. A laser machine costs Can$35,000.00–
200,000.00, and each machine can fully treat 20,000 patients for
COVID-19. In comparison, an IL-6 antagonist costs US$1000.00
per injection, and each patient would need 3–6 injections for com-
plete COVID-19 treatment. Treating 20,000 patients would cost
US$ 60,000,000.00–US$ 120,000,000.00.
Based on this information, LLLT will accelerate recovery from COVID-
19 and will get patients off ventilator support and out of the ICU more
rapidly. This could significantly decompress our severely overburdened
health care systems.
Therapeutic technique and dosage of LLLT
Laser dose is the amount of energy delivered per second per cm2. The effect
of laser therapy is related to the amount of laser energy per cm2. The Arndt-
Schultz Law is considered the standard to describe the dose dependent
effects of LLLT [42]. The minimum therapeutic dose for a bio-stimulatory
effect for red and infrared laser is 0.01 J/cm2 while for ultraviolet, blue,
green laser it is 0.001 J/cm2. LLLT has a noticeable biphasic dose response.
The effective stimulation dose is 1 J/cm2 on the target tissue. Doses greater
than 10 J/cm2 produces inhibitory effects. The inhibitory effects are used
in conditions requiring inhibition and suppression [2].
FIGURE 2
The effects of SARS-CoV-2 versus LLLT on cytokine storm and lung tissue.
Low level laser therapy for COVID-19
Can J Respir Ther Vol 56 5
Therapeutic protocol: early phase of COVID-19: (Figure 3, Table 2)
Laser parameters:
Laser type: infrared laser (780–900 nm), or red laser (630–660 nm)
Average power: 50–100 mW
Dose: 4–6 J/cm2
Area: 10 cm2
Time: 1–2 minutes/cm2
Sessions: 3–8 once-daily sessions
Laser probe positions:
Intranasal: 2 minutes, noncontact technique
Over right and left tonsils: transcutaneous (place laser over the
skin)
Over the trachea: transcutaneous
Over the veins in the cubital areas: transcutaneous blood laser
therapy, 10–15 minutes
Therapeutic protocol: medium–severe phase of COVID-19:
(Figure 3, Table 3)
Laser parameters:
Laser type: infrared laser (780–900 nm) or red laser (630–660 nm)
Average power: 50–100 mW
Dose: 6–10 J/cm2
Area: 10 cm2
Time: 2–3 minutes/cm2
Sessions: 3–10 once-daily sessions
Laser Probe Positions:
Over the lungs: bilaterally over apical, middle, and lower lobes and
front and back of thorax, transcutaneous over the intercostal spaces
Over the trachea: transcutaneous
Over the bronchus: upper mediastinal area, transcutaneous
Over right and left tonsils: transcutaneous
Over the veins in the cubital areas: transcutaneous blood laser
therapy; 10–15 minutes
Contraindications and side effects of LLLT [42]
Although LLLT is safe and noninvasive and there are no reports of muta-
genicity, genotoxicity, or carcinogenicity of LLLT after 60 years of its use.
However, there are some contraindications:
work over the site of tumors and cancer;
benign tumors with possibility of converting to malignant tumors;
FIGURE 3
LLLT for COVID-19.
TABLE 2
Therapeutic protocol: Early phase of COVID-19
Laser system parameters
Wavelengths Infrared laser (780–900 nm), or red
laser (630–660 nm)
Average power 50–100 mW
Dose 4–6 J/cm2
Area 10 cm2
Sessions 3–8 once-daily sessions
Laser probe positions
Intranasal:
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Noncontact technique
Over right and left tonsils
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Transcutaneous
(place laser over the skin)
Over the trachea
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Transcutaneous
Over the veins in the cubital areas
8 minute/cm2 (100 mW)
15 minutes/cm2 (50 mW)
Transcutaneous blood laser therapy
Soheila Mokmeli and Mariana Vetrici
6 Can J Respir Ther Vol 56
the first 3 months of pregnancy (in the second and third trimes-
ters, avoid work on abdominal and spine area); and
light sensitivity conditions.
Precautions [42]
epiphyseal line in children;
glands: avoid ovaries, testes;
in patients with severe end organ damage: heart, kidney, liver, and
lung;
epilepsy: the possibility of ner ve discharge is increased in LLLT,
especially with low-frequency protocols, 5–10 HZ.
Side effects of LLLT
Optical side effects
Because of the high intensity of lasers and the absorption of its wave-
lengths by different parts of ocular system, there is a possibility of dam-
age to the eyes. It is important to use protective glasses that can absorb
the specific wavelength. Protective glasses for each wavelength are differ-
ent; therefore, choose the protective goggles specified for each wave-
length. Both therapists and clients should wear protective goggles [42].
Early sense of healing
The analgesic effect of laser manifests earlier than its healing effect, and
the patients feel better because of this, but the actual tissue damage has
not yet healed. Patients feel relaxed and more energetic because the pain
is gone. However, they must allow enough time for recovery [42].
Fatigue and tiredness
Fatigue is the most common symptom following LLLT. This is due to
hormonal and metabolite changes after laser therapy that increase
expression natural pain killers like endorphins and enkephalins. These
metabolites induce relaxation and sleepiness [42].
Low blood pressure and dizziness
Very rarely, when the treated area is close to large blood vessels, a patient
may experience a temporary drop in the blood pressure and orthostasis.
This is due to vasodilatation and increased circulation to the limbs. To
avoid dizziness, it is recommended that patients drink fluids before
LLLT, and then wait for a few minutes before getting up from the supine
position [42].
CONCLUSION
COVID-19 is potentially lethal because of cytokine storm and ARDS.
Although most patients who contract COVID-19 may recover at home,
a significant proportion require hospitalization and (or) ICU treat-
ment. Many of the patients that are placed on ventilators succumb to
the disease despite the best treatment practices. Often, patients are
maintained on ventilators for longer than expected, and this may con-
tribute to ventilator induced lung injury while depleting the patient’s
convalescent resources. Modulation of inflammatory factors and a
boost to healing are necessary to help patients come off the ventilators.
LLLT is a safe and noninvasive modality that has been used for decades
in pain management, wound healing, and health conditions including
diseases of the respiratory tract. LLLT was combined successfully with
standard medical care to optimize response to treatments, reduce
inflammation, promote healing, and accelerate recovery times.
Scientific evidence shows that LLLT attenuates the inflammator y cyto-
kines and chemokines in cytokine storm at multiple levels. In addition,
LLLT promotes apoptosis of inflammatory cells and protects alveolar
cells from damage. These findings suggest that LLLT is a feasible
modality in the treatment of ARDS. LLLT can be added to the conven-
tional treatment in COVID-19 at different stages of the disease.
Because of its anti-inflammatory effect, and ability to shorten recovery
times, LLLT can reduce the need of ventilators in the healing process.
Clinical trials are necessary to objectively evaluate the effect of LLLT
on COVID-19 treatment and recovery.
Contributors
Soheila Mokmeli and Mariana Vetrici contributed to the conception
and design of the work.
Competing interests
All authors have completed the ICMJE uniform disclosure form at www.
icmje.org/coi_disclosure.pdf and declare: no financial relationships
with any organizations that might have an interest in the submitted work
in the previous 3 years; no other relationships or activities that could
appear to have influenced the submitted work.
Ethical approval
Informed consent was obtained from all participants.
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TABLE 3
Therapeutic protocol: medium–severe phase of COVID-19
Laser system parameters
Wavelengths Infrared laser (780–900 nm), or red laser
(630–660 nm)
Average power 50–100 mW
Dose 6–10 J/cm2
Area 10 cm2
Sessions 3–10 once-daily sessions
Laser probes positions
Intranasal:
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Noncontact technique
Over right and left tonsils
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Transcutaneous
(place laser over the skin)
Over the trachea
1 minute/cm2 (100 mW)
2 minutes/cm2 (50 mW)
Transcutaneous
Over the veins in the cubital
areas
8 minute/cm2 (100 mW)
15 minutes/cm2 (50 mW)
Transcutaneous blood laser therapy
Over the lungs
1:30–2 minute/cm2 (100 mW)
2–3 minutes/cm2 (50 mW)
Bilaterally over apical, middle, and lower
lobes, front and back of thorax; transcuta-
neous over the intercostal spaces
Over the bronchus
1:30–2 minute/cm2 (100 mW)
2–3 minutes/cm2 (50 mW)
Upper mediastinal area: transcutaneous
Low level laser therapy for COVID-19
Can J Respir Ther Vol 56 7
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... In the last decades, light has been increasingly applied in research, survey, treatment, and therapy of biological objects (considering here the term light for near-ultraviolet (UV), visible, and nearinfrared (NIR) irradiation); it is named as low-level laser therapy (LLLT) and more generally as photobiomodulation (PBM) or photobiomodulation therapy (PBMT) (1,2). There are few known independent light-sensitive cellular pathways as the activation of ion channels on cell membrane and endoplasmic reticulum (3,4), though, light principally interacts with mitochondria, which is the main source of cellular reactive oxygen species (ROS) (5)(6)(7). ...
... To date, the most discussed photoacceptor is cytochrome c oxidase (CCO) (6,13). CCO absorbs red/NIR light within wavelengths ranging between 600-1000 nm, resulting in the activation of metabolic process as well as migration and proliferation of various cell types: neurons (650-660/808 nm at 3-90 J/cm 2 (3,4,14), fibroblasts (660 nm at 5 J/cm 2 (15), 660 nm at 3-8 J/cm 2 (16), 809 nm at 1.96-7.84 J/cm 2 (17)), endothelial cells (635 nm at 24 J/cm 2 (18), 650 nm at 30 J/cm 2 (19), 665 and 675 nm at 10 J/cm 2 (20), 808 nm at 60 J/cm 2 (21)), stem cells (660 nm (22,23) and 808 nm at 3 J/cm 2 (24)), keratinocytes (780 nm at 0.45-0.95 ...
... To date, the most discussed photoacceptor is cytochrome c oxidase (CCO) (6,13). CCO absorbs red/NIR light within wavelengths ranging between 600-1000 nm, resulting in the activation of metabolic process as well as migration and proliferation of various cell types: neurons (650-660/808 nm at 3-90 J/cm 2 (3,4,14), fibroblasts (660 nm at 5 J/cm 2 (15), 660 nm at 3-8 J/cm 2 (16), 809 nm at 1.96-7.84 J/cm 2 (17)), endothelial cells (635 nm at 24 J/cm 2 (18), 650 nm at 30 J/cm 2 (19), 665 and 675 nm at 10 J/cm 2 (20), 808 nm at 60 J/cm 2 (21)), stem cells (660 nm (22,23) and 808 nm at 3 J/cm 2 (24)), keratinocytes (780 nm at 0.45-0.95 ...
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The effect of UV/visible/NIR light (380/450/530/650/808/1064 nm) on ROS generation, mitochondrial activity, and viability is experimentally compared in human neuroblastoma cancer cells. The absorption of photons by mitochondrial photoacceptors in Complexes I, III, IV is in‐detail investigated by sequential blocking with selective pharmaceutical blockers. Complex I absorbs UV/blue light by heme P450, resulting in a very high rate (14 times) of ROS generation leading to cell death. Complex III absorbs green light, by cytochromes b, c1 and c, and possesses less ability for ROS production (7 times), so that only irradiation lower than 10 mW/cm2 cause an increase in cell viability. Complex IV is well‐known as the primary photoacceptor for red/NIR light. Light of 650/808 nm at 10–100 mW/cm2 generates a physiological ROS level about 20% of a basal concentration, which enhance mitochondrial activity and cell survival. While, 1064 nm light does not show any distinguished effects. Further, ROS generation induced by low‐intensity red/NIR light is compared in neurons, immune and cancer cells. Red light seems to more rapidly stimulate ROS production, mitochondrial activity, and cell survival than 808 nm. At the same time, different cell lines demonstrate slightly various rates of ROS generation, peculiar for their cellular physiology.
... Therapeutic protocol: COVID-19 moderatesevere forms(23) Clinical trials have shown that the laser used in COVID-19 pneumonia has reduced respiratory symptoms by normalizing respiratory function; the recovery time has been significantly shortened and all blood, immunological and radiological parameters have improved(24). We mention the post-treatment results for the patients in the first randomized pilot study that involved patients with confirmed COVID-19, conducted in August 2020 by Dr. Sigman: PCR normalized; from 15.1 mg/dL to 1.23 mg/dL 7. Ferritin decreased from 359 ng/mL to 175 ng/mL 8. Clinical recovery was a total of 3 weeks, while the mean time is usually 6 to 8 weeks. ...
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Introduction. An unprecedented public health crisis has been triggered worldwide by SARS-CoV-2’s high contagiosity and it’s mortality rates of 1-5%. Although the majority of COVID-19 cases have a good outcome, there is a small percentage that develop severe pneumonia and citokine storm and may be in the need of mechanical ventilation. Methods. Identifying the exact drivers of the excessive inflammation and the biomarkers that can predict a hyperinflammatory response to SARS-CoV-2 would be extremly helpful in finding efficient anti-inflammatory interventions that may stop the progression to acute respiratory distress syndrome (ARDS). Results. In the search for such interventions we have identified the promising effect of low level LASER therapy (LLLT) on lung inflammation from COVID-19 pneumonia. Due to its well known anti-inflammatory effect and modulatory activity on immune cells, laser therapy may be able to decrease lung and systemic inflammation without affecting lung function in acute lung lesions, relieve respiratory symptoms, normalize respiratory function and stimulate the healing process of lung tissue. The recovery time may also be significantly shortened and all blood, immunological and radiological parameters may improve. Conclusions. This findings need further confirmation from clinical trials but we are hopeful for their contribution on the global battle against COVID-19 pandemic.
... Therapeutic protocol: COVID-19 moderatesevere forms(23) Clinical trials have shown that the laser used in COVID-19 pneumonia has reduced respiratory symptoms by normalizing respiratory function; the recovery time has been significantly shortened and all blood, immunological and radiological parameters have improved(24). We mention the post-treatment results for the patients in the first randomized pilot study that involved patients with confirmed COVID-19, conducted in August 2020 by Dr. Sigman: PCR normalized; from 15.1 mg/dL to 1.23 mg/dL 7. Ferritin decreased from 359 ng/mL to 175 ng/mL 8. Clinical recovery was a total of 3 weeks, while the mean time is usually 6 to 8 weeks. ...
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Introduction. An unprecedented public health crisis has been triggered worldwide by SARS-CoV-2’s high contagiosity and it’s mortality rates of 1-5%. Although the majority of COVID-19 cases have a good outcome, there is a small percentage that develop severe pneumonia and citokine storm and may be in the need of mechanical ventilation. Methods. Identifying the exact drivers of the excessive inflammation and the biomarkers that can predict a hyperinflammatory response to SARS-CoV-2 would be extremly helpful in finding efficient anti-inflammatory interventions that may stop the progression to acute respiratory distress syndrome (ARDS). Results. In the search for such interventions we have identified the promising effect of low level LASER therapy (LLLT) on lung inflammation from COVID-19 pneumonia. Due to its well known anti-inflammatory effect and modulatory activity on immune cells, laser therapy may be able to decrease lung and systemic inflammation without affecting lung function in acute lung lesions, relieve respiratory symptoms, normalize respiratory function and stimulate the healing process of lung tissue. The recovery time may also be significantly shortened and all blood, immunological and radiological parameters may improve. Conclusions. This findings need further confirmation from clinical trials but we are hopeful for their contribution on the global battle against COVID-19 pandemic. Keywords: SARS-CoV-2, pneumonia, low LASER level therapy, anti-inflammatory effect, citokine storm
... LLLT reduces inflammation at multiple levels and may be an effective strategy to control cytokine storm [14][15][16][17]. The use of adjunctive LLLT or PBMT has been recommended as a potential treatment modality to reduce cytokine storm, ARDS, and the need for ventilators in COVID-19 [18,19]. ...
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Introduction: COVID-19 poses a higher risk of complications in obese patients due to low respiratory system compliance, increased inflammatory cytokines, and an activated immune system secondary to excess adiposity. Low level laser therapy (LLLT) has significant anti-inflammatory effects and reduces inflammatory cytokines. It is noninvasive and approved for pain management and musculoskeletal injuries. Data from human and experimental animal models of respiratory tract disease suggests that LLLT reduces inflammation and promotes lung healing. Case and outcomes: A morbidly obese 32-year-old Asian female with severe COVID-19 received four consecutive once-daily LLLT sessions via a laser scanner. Pulsed 808 nm and 905 nm laser beams were delivered over the posterior chest for 28 min. The patient was evaluated before and after LLLT by radiological assessment of lung edema (RALE) on chest X-ray, oxygen requirements and saturation, pneumonia severity indices (SMART-COP and Brescia-COVID), blood inflammatory markers (interleukin-6, ferritin, and C-Reactive protein (CRP)). Prior to treatment, oxygen saturation (SpO2) via pulse oximetry was 88%-93% on 5-6 L oxygen. Following LLLT, SpO2 increased to 97%-99% on 1-3 L oxygen. Reductions in RALE score from 8 to 3, Brescia-COVID from 4 to 0, and SMART-COP from 5 to 0 were observed. Interleukin-6 decreased from 45.89 to 11.7 pg/mL, ferritin from 359 to 175 ng/mL, and CRP from 3.04 to 1.43 mg/dL. Post-treatment, the patient noted appreciable improvement in respiratory symptoms. Conclusion: Following LLLT our patient showed improvement over a few days in respiratory indices, radiological findings, inflammatory markers, and patient outcomes. This report suggests that adjunct LLLT can be safely combined with conventional treatment in patients with severe COVID-19 and morbid obesity.
... Infrared (IR)-PBMT on COVID-19 was investigated in recent studies using pulsed low-level laser 808 nm and 905 nm. 8,9 Here, we report the use of non-coherent light-emitting diodes (LED) 630 nm and 660 nm simultaneously with +15 nm spectral shift (Table 1). ...
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Given the magnitude of the viral pandemic, we report the successful treatment of two early clinical cases of acute infectious respiratory syndrome addressed with Photobiomodulation and, welcome the scientific community interest in these early findings, clinical basis for further research.
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The coronavirus disease-19 (COVID-19) caused by SARS-CoV-2 infection can lead to a series of clinical settings from non-symptomatic viral carriers/spreaders to severe illness characterized by acute respiratory distress syndrome (ARDS)1,2. A sizable part of patients with COVID-19 have mild clinical symptoms at the early stage of infection, but the disease progression may become quite rapid in the later stage with ARDS as the common manifestation and followed by critical multiple organ failure, causing a high mortality rate of 7-10% in the elderly population with underlying chronic disease1-3. The pathological investigation in the lungs and other organs of fatal cases is fundamental for the mechanistic understanding of severe COVID-19 and the development of specific therapy in these cases. Gross anatomy and molecular markers allowed us to identify, in two fatal patients subject to necropsy, the main pathological features such as exudation and hemorrhage, epithelium injuries, infiltration of macrophages and fibrosis in the lungs. The mucous plug with fibrinous exudate in the alveoli and the activation of alveolar macrophages were characteristic abnormalities. These findings shed new insights into the pathogenesis of COVID-19 and justify the use of interleukin 6 (IL6) receptor antagonists and convalescent plasma with neutralizing antibodies against SARS-CoV-2 for severe patients. Authors Chaofu Wang, Jing Xie, Lei Zhao, Xiaochun Fei, Heng Zhang, and Yun Tan contributed equally to this work. Authors Chaofu Wang, Jun Cai, Rong Chen, Zhengli Shi, and Xiuwu Bian jointly supervised this work.
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Currently there is no effective antiviral therapy for SARS-CoV-2 infection, which frequently leads to fatal inflammatory responses and acute lung injury. Here, we discuss the various mechanisms of SARS-CoV-mediated inflammation. We also assume that SARS-CoV-2 likely shares similar inflammatory responses. Potential therapeutic tools to reduce SARS-CoV-2-induced inflammatory responses include various methods to block FcR activation. In the absence of a proven clinical FcR blocker, the use of intravenous immunoglobulin to block FcR activation may be a viable option for the urgent treatment of pulmonary inflammation to prevent severe lung injury. Such treatment may also be combined with systemic anti-inflammatory drugs or corticosteroids. However, these strategies, as proposed here, remain to be clinically tested for effectiveness.
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Since the SARS outbreak 18 years ago, a large number of severe acute respiratory syndrome-related coronaviruses (SARSr-CoV) have been discovered in their natural reservoir host, bats1–4. Previous studies indicated that some of those bat SARSr-CoVs have the potential to infect humans5–7. Here we report the identification and characterization of a novel coronavirus (2019-nCoV) which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started from 12 December 2019, has caused 2,050 laboratory-confirmed infections with 56 fatal cases by 26 January 2020. Full-length genome sequences were obtained from five patients at the early stage of the outbreak. They are almost identical to each other and share 79.5% sequence identify to SARS-CoV. Furthermore, it was found that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. The pairwise protein sequence analysis of seven conserved non-structural proteins show that this virus belongs to the species of SARSr-CoV. The 2019-nCoV virus was then isolated from the bronchoalveolar lavage fluid of a critically ill patient, which can be neutralized by sera from several patients. Importantly, we have confirmed that this novel CoV uses the same cell entry receptor, ACE2, as SARS-CoV.
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Background: A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods: All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings: By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0-58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0-13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation: The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding: Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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Background and purpose: Severe influenza A virus (IAV) infections are associated with damaging hyperinflammation that can lead to mortality. There is an urgent need to identify new therapeutics to treat severe and pathogenic IAV infections. The repurposing of drugs with an existing and studied pharmacokinetic and safety profile is a highly attractive potential strategy. We have previously demonstrated that the NLRP3 inflammasome plays a temporal role during severe IAV infection with early protective responses, however, subsequent dysregulation leads to excessive inflammation, contributing to disease severity. Experimental approach: We evaluated the use of existing drugs to target P2X7 receptor signalling and dampen NLRP3 inflammasome responses during severe IAV infection. The ability of Probenecid and AZ11645373 to limit NLRP3 inflammasome-dependent IL-1β secretion in vitro was evaluated. The effectiveness of Probenecid and AZ11645373 treatment at reducing hyperinflammation and disease during severe IAV infection was demonstrated. Key results: Probenecid and AZ11645373 treatment of macrophages in vitro diminished NLRP3 inflammasome-dependent IL-1β secretion. Intranasal therapeutic treatment of mice displaying severe influenza disease with Probenecid or AZ11645373 reduced pro-inflammatory cytokine production, cellular infiltrates in the lung and provided protection against disease. Importantly, Probenecid and AZ11645737 could be administered at either early or late stage of disease and provide therapeutic efficacy. Conclusions and implications: Our study demonstrates that the anti-inflammatory drugs Probenecid and AZ11645373, which have documented pharmacokinetics and safety profiles in humans, are effective at dampening hyperinflammation and severe influenza disease providing potentially new therapeutic strategies for treating severe or pathogenic IAV infections.
Article
Purpose: To evaluate the effect of low-level laser therapy (LLLT) on an experimental model of ventilator-induced lung injury (VILI). Methods: 24 adult Wistar rats were randomized in four groups: protective mechanical ventilation (PMV), PMV+laser, VILI and VILI+laser. The animals of the PMV and VILI groups were ventilated with tidal volume of 6 and 35 ml/Kg, respectively for 90 minutes. After the first 60 minutes of ventilation, the animals of the laser groups were irradiated (808 nm, 100 mW power density, 20 J/cm² energy density, continuous emission mode, and exposure time 5s) and after 30 minutes of irradiation, the animals were euthanized. Lung samples were removed to morphological analysis, bronchoalveolar lavage (BAL) and RT-qPCR technique. Results: The VILI group showed greater acute lung injury (ALI) score with an increase in neutrophil infiltration, higher neutrophil count in the BAL fluid and greater cytokine mRNA expression compared to the PMV groups (p<0.05). The VILI+laser group when compared to the VILI group showed lower ALI score (0.35 ± 0.08 vs. 0.54 ± 0.13, p<0.05), alveolar neutrophil infiltration (7.00 ± 5.73 vs. 21.50 ± 9.52, p<0.05), total cell count (1.90 ± 0.71 vs. 4.09 ± 0.96 x105, p<0.05) and neutrophil count in the BAL fluid (0.60 ± 0.37 vs. 2.28 ± 0.48 x105, p<0.05). Moreover, LLLT induced a decrease in pro-inflammatory and an increase of anti-inflammatory mRNA levels compared to the VILI group (p<0.05). Conclusion: LLLT reduced the inflammatory response in an experimental model of VILI.
Article
Idiopathic pulmonary fibrosis (IPF) is a progressive and chronic inflammatory disease with a poor prognosis and very few available treatment options. Low-level laser therapy (LLLT) has been gaining prominence as a new and effective anti-inflammatory and immunomodulatory agent. Can lung inflammation and the airway remodeling be regulated by LLLT in an experimental model of IPF in C57Bl/6 mice? The present study investigated if laser attenuates cellular migration to the lungs, the airway remodeling as well as pro-fibrotic cytokines secretion from type II pneumocytes and fibroblasts. Mice were irradiated (780 nm and 30 mW) and then euthanized fifteen days after bleomycin-induced lung fibrosis. Lung inflammation and airway remodeling were evaluated through leukocyte counting in bronchoalveolar lavage fluid (BALF) and analysis of collagen in lung, respectively. Inflammatory cells in blood were also measured. For in vitro assays, bleomycin-activated fibroblasts and type II pneumocytes were irradiated with laser. The pro- and anti-inflammatory cytokines level in BALF as well as cells supernatant were measured by ELISA, and the TGFβ in lung was evaluated by flow cytometry. Lung histology was used to analyze collagen fibers around the airways. LLLT reduced both migration of inflammatory cells and deposition of collagen fibers in the lungs. In addition, LLLT downregulated pro-inflammatory cytokines and upregulated the IL-10 secretion from fibroblasts and pneumocytes. Laser therapy greatly reduced total lung TGFβ. Systemically, LLLT also reduced the inflammatory cells counted in blood. There is no statistical difference in inflammatory parameters studied between mice of the basal group and the laser-treated mice. Data obtained indicate that laser effectively attenuates the lung inflammation, and the airway remodeling in experimental pulmonary fibrosis is driven to restore the balance between the pro- and anti-inflammatory cytokines in lung and inhibit the pro-fibrotic cytokines secretion from fibroblasts.