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Convergence of air pollutant-induced redox-sensitive signals in the dendritic cells contributes to asthma pathogenesis.

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Convergence of air pollutant-induced redox-sensitive signals in the dendritic cells contributes to asthma pathogenesis.

Toxicol Lett. 2015 May 27;

Authors: Li N, Buglak N

Abstract
Exposure to airborne particulate matter (PM) is a major risk factor for allergic airway inflammation such as asthma. Many of the PM components (i.e., polycyclic aromatic hydrocarbons and metals) are redox-active and capable of inducing cellular oxidative stress and injuries including inflammation and cell death. Airway epithelial cells and antigen-presenting dendritic cells (DC) are the major and direct targets of inhaled PM. The epithelial cells can further enhance the DC response to allergen and PM through several immune regulatory cytokines including thymic stromal lymphopoietin (TSLP), IL-33, and IL-25. Among these cytokines TSLP is particularly relevant to the mechanisms by which particulate air pollutants contribute to asthma pathogenesis. Studies have found that TSLP released by PM-exposed human airway epithelial cells could polarize the DC towards a T-helper 2 immune response, which is one of the key immunological mechanisms in asthma pathogenesis. The convergence of regulatory signals generated by PM-induced oxidative stress in DC and the interactions among them may be one of the major mechanisms that are specifically related to the contribution of PM towards asthma pathogenesis.

PMID: 26026960 [PubMed – as supplied by publisher]

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Cleaner air contributes to fewer asthma, emphysema deaths – CBC.ca


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Cleaner air contributes to fewer asthma, emphysema deaths
CBC.ca
Air pollution controls help to save lives, a U.S. study suggests, as death rates from emphysema, asthma and pneumonia fell dramatically as air quality improved.. Most research has focused on a specific air pollutant or a couple of pollutants over short …
Air pollution controls linked to lower death rates in North CarolinaMedical Xpress

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Altered CD38/Cyclic ADP-Ribose Signaling Contributes to the Asthmatic Phenotype.

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Altered CD38/Cyclic ADP-Ribose Signaling Contributes to the Asthmatic Phenotype.

J Allergy (Cairo). 2012;2012:289468

Authors: Jude JA, Dileepan M, Panettieri RA, Walseth TF, Kannan MS

Abstract
CD38 is a transmembrane glycoprotein expressed in airway smooth muscle cells. The enzymatic activity of CD38 generates cyclic ADP-ribose from ?-NAD. Cyclic ADP-ribose mobilizes intracellular calcium during activation of airway smooth muscle cells by G-protein-coupled receptors through activation of ryanodine receptor channels in the sarcoplasmic reticulum. Inflammatory cytokines that are implicated in asthma upregulate CD38 expression and increase the calcium responses to contractile agonists in airway smooth muscle cells. The augmented intracellular calcium responses following cytokine exposure of airway smooth muscle cells are inhibited by an antagonist of cyclic ADP-ribose. Airway smooth muscle cells from CD38 knockout mice exhibit attenuated intracellular calcium responses to agonists, and these mice have reduced airway response to inhaled methacholine. CD38 also contributes to airway hyperresponsiveness as shown in mouse models of allergen or cytokine-induced inflammatory airway disease. In airway smooth muscle cells obtained from asthmatics, the cytokine-induced CD38 expression is significantly enhanced compared to expression in cells from nonasthmatics. This differential induction of CD38 expression in asthmatic airway smooth muscle cells stems from increased activation of MAP kinases and transcription through NF-?B, and altered post-transcriptional regulation through microRNAs. We propose that increased capacity for CD38 signaling in airway smooth muscle in asthma contributes to airway hyperresponsiveness.

PMID: 23213344 [PubMed – in process]

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