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Lower natural killer cell cytotoxicity in smokers may be mediated by epithelial cells
Author(s) -
Muller Loretta,
Brighton Luisa E.,
Jaspers Ilona
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.645.1
Subject(s) - cytotoxicity , granzyme , immunology , granzyme b , context (archaeology) , natural killer cell , biology , cell , lymphokine activated killer cell , cytotoxic t cell , nk 92 , interleukin 21 , cell culture , in vitro , chemistry , immune system , perforin , t cell , biochemistry , paleontology , genetics
Cigarette smoking is a risk factor for viral infections, yet the mechanisms underlying this susceptibility remain unknown. Natural killer (NK) cells play an important role in fighting influenza and signals from epithelial cells (EC) likely regulate NK cell activity. We have previously shown that markers of cytotoxicity are reduced in nasal NK cells from smokers after influenza infection. This study investigated if human EC from smokers and nonsmokers differentially affect NK cell activity in the context of influenza infection. EC were infected with influenza and subsequently co‐cultured with NK cells. NK cells were also incubated with apical washes and basolateral supernatants of EC to identify the role of soluble mediators. At baseline, co‐culturing NK cells either directly with smoker EC or stimulating with basolateral supernatants from these cells reduced markers of cytotoxicity. Similarly, after influenza infection markers of cytotoxicity as well as levels of IFN‐γ, IL‐4 and granzyme B were decreased in NK cells incubated with basolateral supernatants of smoker EC. Co‐culturing NK cells with EC from smokers reduced markers of cytotoxicity in NK cells through a potential mechanism involving EC‐derived soluble mediators. Thus, EC‐mediated modification of NK cell activity may contribute to the higher susceptibility to influenza infections seen in smokers. The work was supported by NIH, EPA and FAMRI.