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- W4313387726 abstract "Abstract Bronchiolitis is common in smokers and we hypothesized that this may be due to impaired sensing of bacterial components via TLR2 and TLR4 by smokers’ alveolar macrophages (AM). AM and PBMC obtained from smokers and non-smoking volunteers were stimulated with TLR2 and TLR4 agonists, Pam3Cys and LPS, and expression of cytokines and activation of intracellular intermediates were examined. Smokers’ AM exhibited suppressed gene expression and secretion of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IFN-γ and chemokines IL-8 and RANTES upon stimulation with LPS and Pam3Cys, whereas expression of anti-inflammatory cytokines IL-10 and IL-1RA was not affected. Comparable expression levels of these cytokines and chemokines were detected in PBMC obtained from smokers and non-smokers, indicating that the suppressive effect of smoking is restricted to the lung. TLR2/4-inducible phosphorylation of IRAK-1 and p38, and IκB-α degradation were markedly inhibited in smokers’ AM, whereas expression levels of TLR2, TLR4, CD14, MD-2 mRNA, and TLR4 protein, were not significantly changed. These results indicate that smoking induces a state of tolerance in AM manifested by suppression of TLR2/4-induced signaling that may underlie bronchiolitis associated with smoking. This work was supported by grants from Philip Morris USA Inc. and Philip Morris International, OTRD/University of Maryland, Baltimore, and NIH grants AI059524 (AEM) and AI44936 (SNV)." @default.
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- W4313387726 date "2007-04-01" @default.
- W4313387726 modified "2023-09-25" @default.
- W4313387726 title "SMOKING INHIBITS EXPRESSION OF PROINFLAMMATORY CYTOKINES AND ACTIVATION OF IRAK-1, p38 AND NF-κB IN ALVEOLAR MACROPHAGES STIMULATED WITH TLR2 AND TLR4 AGONISTS (40.6)" @default.
- W4313387726 doi "https://doi.org/10.4049/jimmunol.178.supp.40.6" @default.
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