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Obese individuals demonstrate a defective response to influenza A virus infection compared with healthy weight individuals
Author(s) -
Paich Heather,
Karlsson Erik,
Sheridan Patricia,
Beck Melinda
Publication year - 2011
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.25.1_supplement.222.4
Subject(s) - immunology , peripheral blood mononuclear cell , immune system , cd8 , medicine , virus , granzyme b , tumor necrosis factor alpha , influenza a virus , cytokine , cytotoxic t cell , cytolysis , virology , biology , in vitro , biochemistry
Obesity has recently been identified as an independent risk factor for increased morbidity and mortality from novel H1N1 pandemic influenza. To investigate possible immunological reasons for this increased susceptibility, we isolated peripheral blood mononuclear cells (PBMCs) from healthy weight and obese adults and stimulated them ex vivo with influenza A virus. Following an 18 hour stimulation, PBMCs from obese adults produced fewer activated CD8 + T cells expressing interferon‐γ and granzyme B compared with healthy weight adults, suggesting an impairment in activation and cytolytic function. Functional CD8 + T cells are necessary both for protection from and response to influenza A virus infection. In addition, the production of interleukin 10 and tumor necrosis factor alpha was lower in PBMC culture supernatants from obese adults, compared with healthy weight adults, suggesting deficient production of essential pro‐inflammatory and anti‐inflammatory cytokines that function to appropriately regulate the immune response to an influenza virus infection. Taken together, our data suggest that CD8 + T cells from obese adults are defective in both activation and cytolytic function and influenza stimulated PBMCs fail to produce the appropriate cytokine milieu for an optimal response to influenza A virus infection, which may provide a novel mechanism for the increased susceptibility to H1N1 due to obesity. Grant Funding Source : RO1AI078090