Cigarette smoke exposure is considered an important negative prognostic factor for chronic rhinosinusitis (CRS) patients. However, there is no clear mechanistic evidence implicating cigarette smoke exposure in the poor clinical evolution of the disease or in the maintenance of the inflammatory state characterizing CRS. This study aimed to evaluate the effects of cigarette smoke exposure on respiratory cilia differentiation.
Mouse nasal septal epithelium cultures grown at an air-liquid interface were used as a model of respiratory epithelium. After 5 days of cell growth, cultures were exposed to air on the apical surface. Additionally, cigarette smoke condensate (CSC; the particulate phase of tobacco smoke) or cigarette smoke extract (CSE; the volatile phase) were diluted in the basolateral compartment in different concentrations. After 15 days of continuous exposure, scanning electron microscopy and immunofluorescence for type IV tubulin were used to determine presence and maturation of cilia. Transepithelial resistance was also recorded to evaluate confluence and physiological barrier integrity.
CSC and CSE impair ciliogenesis in a dose-dependent manner with notable effects in concentrations higher than 30 microg/mL, yielding >70% nonciliation and shorter cilia compared with control. No statistical difference on transepithelial resistance was evident.
CSC and CSE exposure negatively impacts ciliogenesis of respiratory cells at concentrations not effecting transepithelial resistance. The impairment on ciliogenesis reduces the mucociliary clearance apparatus after injury and/or infection and may explain the poor response to therapy for CRS patients exposed to tobacco smoke.
"In our experiments, we investigated the influence of repeated cigarette smoke exposure at non-toxic doses on cilia length in primary normal human bronchiolar epithelial cells. In contrast to other in vitro studies (Brekman et al., 2014; Tamashiro et al., 2009) in which the cells were exposed to cigarette smoke extracts or condensates from the basal side, we exposed them directly at the air–liquid interface in a CULTEX ® RFS module. Native cigarette mainstream smoke of four cigarettes was introduced at five days per week, eight repetitions were done in total. "
"Passive smoke exposure has been evaluated by the U.S. Surgeon General as a cause or exacerbating factor in cardiac, pulmonary, and oncologic diseases for >40 years. It is estimated that 60% of children aged 3–11 years and 40% of nonsmoking adults are exposed to passive smoke, which is known to cause symptoms of nasal irritation.6 Passive smoke exposure has been shown to inhibit upper airway mucociliary clearance,7,8 increase the incidence of sinonasal biofilms,9 promote the sinonasal tissue allergic response,10 and negatively impact sinus surgery clinical outcomes.11,12 Exposure to passive smoke has also been linked to increased incidence and severity of acute and allergic rhinosinusitis.13,14 "
[Show abstract][Hide abstract] ABSTRACT: Background: Prevalence of passive smoke exposure is relatively unknown in chronic rhinosinusitis (CRS). Previous studies have attempted to establish this relationship using subjective, questionnaire-based methodologies to assess smoke exposure, thus introducing the potential for error bias. The purpose of this study was to accurately determine the prevalence of passive smoke exposure in CRS and control patients using hair nicotine levels as a quantitative measure of cigarette smoke exposure. Methods: Hair samples were obtained at time of surgery from 569 patients: 404 undergoing surgery for CRS and 165 controls undergoing surgery for repair of cerebrospinal fluid leak, removal of pituitary tumors, or adenoidectomy from 2007 to 2013. Patient charts were reviewed for reported smoking status. Hair nicotine was quantified using reversed-phase high-performance liquid chromatography. Nonsmoking patients were classified as passive smoke exposed or smoke naïve according to the hair nicotine results. Statistical analysis was performed to test for differences in demographic information and smoke exposure prevalence between CRS, CRS subtypes, and controls. Results: The prevalence of passive smoke exposure in CRS as documented by hair nicotine was lower than previously reported subjective estimates. Passive smoke exposure rates were equivalent between those with CRS versus controls and significantly higher in children. Severity of passive smoke exposure was also equivalent between CRS subsets and controls. Annual passive smoke exposure prevalence did not change over time. Conclusion: There is no clear evidence of avoidance of passive smoke exposure in the CRS population compared with controls. Passive smoke exposure also remained stable over time despite recent regional implementation of smoking bans. Given the constancy of exposure, it is critical that the impact of passive smoke on CRS exacerbation, outcomes, and pathophysiology be evaluated in large-scale clinical studies.
American journal of rhinology & allergy 08/2014; 28(4). DOI:10.2500/ajra.2014.28.4058 · 1.81 Impact Factor
"On the other hand, in COPD patients the impaired mucociliary function may be due to a combination of excessive mucus production, increased viscosity of mucus due to acquired dysfunction of CFTR, and reduced ciliary beating.68-70 It has been shown that respiratory epithelial cells exposed to cigarette smoke extract or condensate showed shorter and 70% fewer cilia compared control cells.71 Although mice exposed to cigarette smoke showed slight increases in ciliary beat frequencies at 6 weeks and 3 mo, it was significantly reduced at 6 mo, and post-mortem examination revealed significant loss of tracheal ciliated cells.72 "
[Show abstract][Hide abstract] ABSTRACT: Airway epithelium contributes significantly to the barrier function of airway tract. Mucociliary escalator, intercellular apical junctional complexes which regulate paracellular permeability and antimicrobial peptides secreted by the airway epithelial cells are the three primary components of barrier function of airway tract. These three components act cooperatively to clear inhaled pathogens, allergens and particulate matter without inducing inflammation and maintain tissue homeostasis. Therefore impairment of one or more of these essential components of barrier function may increase susceptibility to infection and promote exaggerated and prolonged innate immune responses to environmental factors including allergens and pathogens resulting in chronic inflammation. Here we review the regulation of components of barrier function with respect to chronic airways diseases.
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