Role of infection and cytokines in the pathogenesis of chronic obstructive pulmonary disease

Raza, Muhammad W.; Bint, A. J.; Blackwell, C. Caroline

doi:10.1097/00013542-200104000-00005

Cited by 1 publication

(1 citation statement)

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“…Some studies assessed the effects of cigarette smoke in relation to viral or bacterial infections, [1][2][3][4] but not in relation to virusmediated effects on bacterial diseases. Raza et al 4 assessed in vitro the effects of cigarette smoke and respiratory syncytial virus (RSV) infection on induction of TNF-a and NO responses from human peripheral blood monocytes. Cigarette smoke had no effect on TNF-a responses induced by RSV and toxic shock syndrome toxin (TSST).…”

Section: Introductionmentioning

confidence: 99%

Development of an experimental model for assessing the effects of cigarette smoke and virus infections on inflammatory responses to bacterial antigens

et al. 2013

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Interactions among major risk factors associated with bacterial infections were assessed in a model system using surrogates for virus infection; IFN-g, and exposure to cigarette smoke; cigarette smoke extract (CSE), nicotine and cotinine. Cytokine responses elicited by LPS from THP-1 cells in the presence of these components, or combinations of components, were assessed by multiplex bead assay, i.e. IL-1β, IL-6, IL-8, IL-10, TNF-α and IFN-γ. IFN-γ-priming significantly increased pro-inflammatory cytokines induced by LPS. CSE suppressed production of pro-inflammatory cytokines IL-1β, TNF-α and IFN-γ, but enhanced production of IL-8. Nicotine and cotinine suppressed all cytokine responses. In combination, IFN-γ masked the inhibitory effects of CSE. In relation to the objectives of the study, we concluded that (a) IFN-γ at biologically relevant concentrations significantly enhanced pro-inflammatory responses; (b) CSE, nicotine and cotinine dysregulated the inflammatory response and that the effects of CSE were different from those of the individual components, nicotine and cotinine; (c) when both IFN-γ and CSE were present, IFN-γ masked the effect of CSE. There is a need for clinical investigations on the increase in IL-8 responses in relation to exposure to cigarette smoke and increased pro-inflammatory responses in relation to recent viral infection.

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