Abstract
Social disruption stress (SDR) prior to primary influenza A virus (IAV) infection augments memory to IAV re-challenge in a T cell-specific manner. However, the effect of SDR on the primary anti-viral immune response has not been elucidated. In this study, SDR-infected (INF) mice terminated viral gene expression earlier and mounted an enhanced pulmonary IAV-specific CD8 +T cell response versus controls. Additionally, SDR-INF mice had a more pro-inflammatory lung profile prior to and during infection and an attenuated corticosterone response. These data demonstrate neuroendocrine modification of the lung microenvironment and increased antigen-specific T cell activation, clonal expansion and viral control in stress-exposed mice.
Original language | English (US) |
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Pages (from-to) | 34-42 |
Number of pages | 9 |
Journal | Journal of Neuroimmunology |
Volume | 243 |
Issue number | 1-2 |
DOIs | |
State | Published - Feb 29 2012 |
Externally published | Yes |
Bibliographical note
Funding Information:These studies were generously supported by grants from the National Institute of Mental Health RO1 MH46801-17 and the National Institute of Dental and Craniofacial Research T32DE014320-08 to J.F.S. and F30 DE17068-03 to J.W.M.
Keywords
- HPA axis
- Influenza
- Stress
- Sympathetic nervous system
- T cell
- Virus