Year in Review 2012: Acute Lung Injury, Interstitial Lung Diseases, Sleep and Physiology.

Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences,, University of British Columbia, Kelowna, British Columbia, Canada, V1V 2L2.
Respirology (Impact Factor: 3.35). 01/2013; 18(3). DOI: 10.1111/resp.12053
Source: PubMed


The incremental changes made in the definition of ALI/ARDS over the last two decades represent a series of landmark events in the history of the condition. The first description of ARDS (Adult Respiratory Distress Syndrome) established the recognition of this syndrome(1) ; the 1994 AECC (America-European Consensus Conference) definition set the standard for ALI/ARDS clinical trials(2) ; while the new Berlin definition, which has revised the AECC version, is based on 18 years clinical investigation and mechanism exploration, and as a result is a more precise and practical(3) guide for clinical evaluation. The essential components of the new Berlin definition of ARDS are: removal of ALI and division of ARDS into three successive stages (mild, moderate and severe) based on timing, chest imaging, PaO(2) /FiO(2) ratio and level of PEEP applied, with, as previously, exclusion of heart failure or fluid overload. The new definition is based on two large scale databases from 7 medical centers and unifies the understanding of ARDS and establishes a new standard for future clinical trials.

38 Reads
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Acute lung injury (ALI) is a life-threatening syndrome that causes high morbidity and mortality worldwide. ALI is characterized by increased permeability of the alveolar-capillary membrane, edema, uncontrolled neutrophils migration to the lung, and diffuse alveolar damage, leading to acute hypoxemic respiratory failure. Although corticosteroids remain the mainstay of ALI treatment, they cause significant side effects. Agents of natural origin, such as medicinal plants and their secondary metabolites, mainly those with very few side effects, could be excellent alternatives for ALI treatment. Several studies, including our own, have demonstrated that plant extracts and/or secondary metabolites isolated from them reduce most ALI phenotypes in experimental animal models, including neutrophil recruitment to the lung, the production of pro-inflammatory cytokines and chemokines, edema, and vascular permeability. In this review, we summarized these studies and described the anti-inflammatory activity of various plant extracts, such as Ginkgo biloba and Punica granatum, and such secondary metabolites as epigallocatechin-3-gallate and ellagic acid. In addition, we highlight the medical potential of these extracts and plant-derived compounds for treating of ALI.
    10/2013; 2013(7511):576479. DOI:10.1155/2013/576479
  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute lung injury (ALI) is characterized by alveolar injury and uncontrolled inflammation. Mechanisms underlying pathogenesis of ALI are unknown. Regulatory T cells (Tregs), either natural or induced, suppress a variety of physiological and pathological immune responses. In the current study, we investigated whether Tregs were involved in the development of ALI. Proportion of CD4 + CD25 + FoxP3+ Tregs in the peripheral blood of 66 ALI patients and 30 healthy controls were examined by flow cytometry. Data showed that the percentage of Tregs in CD4+ T cells was significantly increased in patients than that in controls (10.8 versus 7.6 %, P = 0.003). Also, compared to those who died during the study, patients who survived presented significantly higher level of Tregs at the time of recruitment (P = 0.041). Since Tim-3 is a negative regulatory molecule and can modulate the function of Tregs, we evaluated Tim-3 level on Tregs and identified upregulation of the molecule in patients than that in controls. Moreover, compared to those who died during the study, patients who survived showed 1.7-fold higher level of Tim-3 on Tregs at the time of recruitment (P < 0.001). These results suggest that Tregs could affect the prognosis of ALI probably due to the upregulation of Tim-3.
    Inflammation 12/2014; 38(3). DOI:10.1007/s10753-014-0096-7 · 2.21 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The present study aimed to investigate the therapeutic effect of monoammonium glycyrrhizinate (MAG) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and possible mechanism. Acute lung injury was induced in BALB/c mice by intratracheal instillation of LPS, and MAG was injected intraperitoneally 1 h prior to LPS administration. After ALI, the histopathology of lungs, lung wet/dry weight ratio, protein concentration, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the BALF were measured by ELISA. The activation of NF-κB p65 and IκB-α of lung homogenate was detected by Western blot. Pretreatment with MAG attenuated lung histopathological damage induced by LPS and decreased lung wet/dry weight ratio and the concentrations of protein in BALF. At the same time, MAG reduced the number of inflammatory cells in lung and inhibited the production of TNF-α and IL-1β in BALF. Furthermore, we demonstrated that MAG suppressed activation of NF-κB signaling pathway induced by LPS in lung. The results suggested that the therapeutic mechanism of MAG on ALI may be attributed to the inhibition of NF-κB signaling pathway. Monoammonium glycyrrhizinate may be a potential therapeutic reagent for ALI.
    Evidence-based Complementary and Alternative Medicine 04/2015; 2015:272474. DOI:10.1155/2015/272474 · 1.88 Impact Factor
Show more

Similar Publications

We use cookies to give you the best possible experience on ResearchGate. Read our cookies policy to learn more.