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Impaired T cell cytokine production during influenza virus infection in diet induced obese mice is not due to an inability to produce cytokines.
Author(s) -
Smith Alexia G.,
Sheridan Patricia A.,
Beck Melinda A.
Publication year - 2007
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.21.5.a375
Subject(s) - cytokine , immunology , immune system , t cell , biology , cytotoxic t cell , cd8 , population , proinflammatory cytokine , medicine , inflammation , biochemistry , environmental health , in vitro
Obesity is associated with immune dysfunction leading to impaired immune responses to challenges with infectious agents, such as influenza virus. Our lab has shown that cytokines important in the cell‐mediated immune response are reduced in the lung and lymph node of obese mice. Specifically, obese mice had diminished levels of IL‐2, IL‐6, and IL‐12, cytokines critical for T cell proliferation and polarization. To determine if this impairment was due to reduced T cell numbers or an inability to produce cytokines, we infected lean and obese C57BL/6 mice with influenza A/PR/8 and analyzed the T cell population using intracellular cytokine staining and flow cytometry. At day 7 post infection, cells from bronchial lavage, lymph node, and spleen were stimulated with PMA, a non‐specific activator of T cells, and stained for the surface markers CD3, CD4 and CD8. IL‐2, IL‐4, and IFNγ production by these cells was detected by intracellular staining. We found that T cell numbers were similar in the lungs and lymphoid tissues of lean and obese mice. Also, PMA stimulated cytokine production was similar between the groups. These data indicate that obese mice are able to initiate T cell responses that are quantitatively similar to lean mice. Interestingly, these data also indicate that T cells maintain the ability to produce cytokines, thus the impaired production during infection is likely due to defective antigen specific responses.