2011
DOI: 10.1165/rcmb.2010-0190oc
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Epithelial Cells from Smokers Modify Dendritic Cell Responses in the Context of Influenza Infection

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Cited by 42 publications
(37 citation statements)
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“…Previous studies conducted by our group have demonstrated that smokers differ in their ability to respond to viral infections, as marked by increased viral replication, suppressed type I interferon responses and decreased activation of NK cells (17,19,25). These responses were associated with DNA methylation of specific antiviral defense response genes in NECs from smokers (19), encouraging us to systematically identify additional changes in DNA methylation that could mediate the impaired antiviral defense responses seen in smokers in vitro and in vivo.…”
Section: Discussionmentioning
confidence: 77%
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“…Previous studies conducted by our group have demonstrated that smokers differ in their ability to respond to viral infections, as marked by increased viral replication, suppressed type I interferon responses and decreased activation of NK cells (17,19,25). These responses were associated with DNA methylation of specific antiviral defense response genes in NECs from smokers (19), encouraging us to systematically identify additional changes in DNA methylation that could mediate the impaired antiviral defense responses seen in smokers in vitro and in vivo.…”
Section: Discussionmentioning
confidence: 77%
“…Differentiation of NECs in vitro takes several weeks, suggesting that the smokinginduced epigenetic changes of ULBP3 are not readily reversible. We have previously shown that virus-induced NK cell activation is reduced in the nasal mucosa of smokers (17). These studies demonstrated that smokers inoculated with liveattenuated influenza virus (LAIV) vaccine had reduced cytotoxic NK cells and markers of activated NK cells in their nasal lavage (17).…”
Section: Discussionmentioning
confidence: 99%
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“…Type I IFN signaling also contributes to the development of secondary bacterial pneumonia after influenza infection (119). In inflammatory diseases such as COPD, higher levels of type I IFN production are observed (120), whereas nasal epithelial cells from smokers have reduced expression of type I IFN receptors, kinases, and reduced type I IFN-dependent cytokines after influenza infection (121).…”
Section: Type I Ifnsmentioning
confidence: 99%