Influenza Virus-Specific Immunological Memory Is Enhanced by Repeated Social Defeat
Open accessAbstract
Immunological memory (MEM) development is affected by stress-induced neuroendocrine mediators. Current knowledge about how a behavioral interaction, such as social defeat, alters the development of adaptive immunity, and MEM is incomplete. In this study, the experience of social disruption stress (SDR) prior to a primary influenza viral infection enhanced the frequency and function of the T cell memory pool. Socially stressed mice had a significantly enlarged population of CD8+ T cells specific for the immunodominant NP366–74 epitope of A/PR/8/34 virus in lung and spleen tissues at 6–12 wk after primary infection (resting memory). Moreover, during resting memory, SDR-MEM mice responded with an enhanced footpad delayed-type hypersensitivity response, and more IFN-γ–producing CD4+ T cells were detected after ex vivo stimulation. When mice were rechallenged with A/PR/8/34 virus, SDR-MEM mice terminated viral gene expression significantly earlier than MEM mice and generated a greater DbNP366–74CD8+ T cell response in the lung parenchyma and airways. This enhancement was specific to the T cell response. SDR-MEM mice had significantly attenuated anti-influenza IgG titers during resting memory. Similar experiments in which mice were primed with X-31 influenza and challenged with A/PR/8/34 virus elicited similar enhancements in the splenic and lung airway DbNP366–74CD8+ T cell populations in SDR-MEM mice. This study demonstrates that the experience of repeated social defeat prior to a primary viral infection significantly enhances virus-specific memory via augmentation of memory T cell populations and suggests that social stressors should be carefully considered in the design and analysis of future studies on antiviral immunity.
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Acute stress enhances antiviral defenses.
“For example, whereas acute stress has been found to enhance antiviral defenses”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Mays et al., 2010
Activation of the classical HPA and ANS stress axes can support or suppress inflammatory and adaptive immune responses in human and animal models, depending on whether it occurs before or after the immunological challenge.
“For example, activation of the classical HPA and ANS stress axes can support or suppress inflammatory and adaptive immune responses in human and animal models, depending, among other factors, on whether it occurs before or after the immunological challenge (274, 371, 474).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [371]
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- Authors
- Mays, J. W., Bailey, M. T., Hunzeker, J. T., Powell, N. D., Papenfuss, T., Karlsson, E. A., Padgett, D. A., & Sheridan, J. F.
- Affiliations
- Section of Oral Biology, College of Dentistry
- Institute for Behavioral Medicine (US)
- Pennsylvania State University (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Sheridan, John F
- ORCID
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-01-18
- Volume
- 184
- Issue
- 4
- Pages
- 2014-2025
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3066050
- OpenAlex
- W2170439791
- Cited by
- 37
- References
- 72
- Citations by year
- 2024: 1 · 2022: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 3 · 2014: 4 · 2013: 3 · 2012: 9
- FWCI
- 4.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- Ohio State University
- National Institute of Mental Health (R01 MH46801-17, R01MH046801)
- National Institute of Dental and Craniofacial Research (F30DE017068, F30 DE17068-03, T32DE014320)
- National Center for Research Resources (K01RR022198)
- Topics
- Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- social defeat, social stress, immunological memory, influenza virus, CD8+ T cells, T cell memory, A/PR/8/34, delayed-type hypersensitivity, interferon-gamma, airway immunity, neuroendocrine stress response, adaptive immunity
- MeSH terms
- Animals, Antigens, Viral, Behavior, Animal, Hypersensitivity, Delayed, Immunologic Memory, Lung, Male, Mice, Inbred C57BL, Orthomyxoviridae Infections, Influenza A virus, Stress, Psychological, CD8-Positive T-Lymphocytes, Epitopes, T-Lymphocyte, Mice, Influenza A Virus, H3N2 Subtype
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