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Mechanisms of social stress enhancement of virus‐specific immune memory
Author(s) -
Mays Jacqueline Wiesehan,
Powell Nicole Damico,
Bailey Michael T,
Padgett David A,
Sheridan John Francis
Publication year - 2008
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.22.1_supplement.857.17
Subject(s) - immune system , virus , cd8 , viral replication , immunology , influenza a virus , virology , immunological memory , social stress , social memory , biology , psychology , medicine , immunity , neuroscience , cognitive science
Murine studies have demonstrated that the experience of social defeat (social disruption stress, SDR) before a primary influenza virus challenge augmented memory CD8 + T cell responses to viral re‐challenge. Patterning of immune memory is established by the immune response to a primary infection, and the present study was designed to investigate potential mechanisms for memory enhancement during a primary challenge. C57BL/6 mice underwent 2 hrs of SDR per night for 6 nights (SDR‐INF group), which entailed introducing an aggressive mouse that physically defeated all resident mice. After night 6 of SDR, mice were intranasally infected with 1 HAU of influenza A/PR/8. Clonal expansion was significantly enhanced in the SDR‐INF group (p<0.05) for the immunodominant D b NP 366 + T cell subset, but not the D b PA 224 + subset. SDR‐INF mice terminated viral replication significantly earlier than INF mice, and expressed more IFNγ mRNA prior to and during A/PR/8 infection. This study suggests that social defeat‐induced enhancement of virus‐specific immune memory occurs at the activation/clonal expansion phase of a primary infection, and is mediated by both cellular and environmental factors. Supported by NIH grants F30DE17068‐02, RO1MH46801‐13, T32DE014320‐04.