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Modulation of natural killer cell activity by restraint stress during an influenza A/PR8 infection in mice

Hunzeker, John, Padgett, David A., Sheridan, Patricia A., Dhabhar, Firdaus S., Sheridan, John F.·2004·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2003.12.010
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Abstract

These experiments were designed to examine the influences of restraint stress (RST) on natural killer (NK) activity and to determine its consequences on influenza A/PR8 (A/PR8) viral replication in mice. The data showed that RST delayed the recruitment of NK1.1+ cells into the lung parenchyma during infection. Quantification of MIP-1alpha and MCP-1 gene expression by real-time PCR revealed that RST suppressed the chemokines responsible for NK cell recruitment into the infected tissue. Additionally, RST suppressed the expression of several macrophage-derived cytokines involved in the effector response of NK cells. IL-15, which is the main cytokine involved in NK cell development and homeostasis, and IL-12, which is important for NK cytotoxicity, were both suppressed. As the NK cell response is an important innate response to control viral replication, we hypothesized that the RST-mediated reduction in NK cell numbers and function would enable viral replication to continue unchecked. In fact, there was enhanced viral replication in the lungs of RST animals. Interestingly, expression of the anti-viral type I interferons (IFN-alpha and IFN-beta) was elevated presumably in response to the elevated viral load in the stressed mice. Together, these data show that RST suppressed expression of the cytokine genes involved in the recruitment and activation of NK cells during an experimental influenza viral infections. The consequence of this effect was diminished NK cell function and enhanced viral replication.

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  • Chronic restraint stress is associated with diminished NK cell function, cytokine secretion, and enhanced viral replication, and its opposing immune effects on myeloid cells compared with RSD can be accounted for by differences in circulating GCs.

    “For example, several studies investigated the immune response to chronic restraint stress and reported diminished natural killer (NK) cell function, cytokine secretion, and enhanced viral replication (Hunzeker et al, 2004;Tseng et al, 2005;Jin et al, 2013).”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Hunzeker et al, 2004

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Authors
Hunzeker, J., Padgett, D. A., Sheridan, P. A., Dhabhar, F. S., & Sheridan, J. F.
Affiliations
  • The Ohio State University (US)
  • University of North Carolina at Chapel Hill (US)
Corresponding author
  • Hunzeker, John
  • Sheridan, John F.
ORCID
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2004-11
Volume
18
Issue
6
Pages
526-535
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2003.12.010
OpenAlex
W2064817595
Cited by
60
References
39
Citations by year
2022: 1 · 2021: 5 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 4 · 2014: 1 · 2013: 2 · 2012: 3
FWCI
1.92
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (MH46801, R01MH046801)
  • National Institute of Allergy and Infectious Diseases (AI48995, R01AI048995)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
restraint stress, natural killer cells, NK1.1+ cells, viral replication, chemokines, MIP-1α, MCP-1, IL-15, IL-12, type I interferon, innate immunity, NK cell recruitment, macrophage-derived cytokines, stress and immunity
MeSH terms
Adaptation, Physiological, Animals, Gene Expression Regulation, Interferon Type I, Killer Cells, Natural, Lung, Male, Mice, Inbred C57BL, Orthomyxoviridae Infections, Influenza A virus, Restraint, Physical, Stress, Psychological, Neuroimmunomodulation, Cytokines, Viral Load, Mice

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