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Cited by 59Stress Responses and CortisolCancer, Stress, Anesthesia, and Immune ResponseImmune Cell Function and Interaction

Stress-induced modulation of NK activity during influenza viral infection: role of glucocorticoids and opioids

Tseng, Raymond J., Padgett, David A., Dhabhar, Firdaus S., Engler, Harald, Sheridan, John F.·2005·Brain, Behavior, and Immunity
DOI 10.1016/j.bbi.2004.07.001
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Abstract

Activation of the hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system by stress has been shown to modulate both innate and adaptive immunity during an experimental influenza A/PR8 viral infection. HPA activation alters levels of glucocorticoids (GC) and opioids which are associated with suppression of lymphoid cellularity and NK activity. These experiments were designed to investigate the role that stress-induced GC and opioids have in modulating NK activity during an influenza viral infection. C57BL/6 mice were treated daily with mifepristone (RU486), a GC receptor antagonist or naltrexone (NTX), a non-specific opioid receptor antagonist. Mice were infected intranasally with A/PR8 virus and underwent daily restraint stress (RST). Phenotypic analysis of splenic cell populations and NK cytotoxicity were assessed at 3 days post-infection. RST of infected mice significantly suppressed splenic CD3(-)DX5+ cellularity and NK cytolytic activity. RU486 administration fully restored splenic NK cellularity but not cytolytic activity. NTX administration restored NK cytolytic activity but not splenic NK cell number. A similar restoration in NK cytolytic activity was observed after administration of beta-funaltrexamine (FNA), a mu-specific opioid receptor antagonist, but not the delta- or kappa-specific opioid receptor antagonists naltrindole or nor-binaltorphimine, respectively. Co-administration of RU486 and NTX restored both NK cellularity and cytolytic activity. The restoration of RST-induced suppression of NK activity by RU486 and NTX or FNA suggests that glucocorticoids modulate NK cellularity and opioids that bind to the mu-opioid receptor modulate NK cytotoxicity during periods of stress and viral infection.

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Crossref · 10.1016/j.bbi.2004.07.001

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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 Tseng et al, 2005

  • Peripheral monocytes traffic to the brain in depressed patients.

    “The first clinical evidence that peripheral monocytes traffic to the brain in depressed patients.”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as [131]

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Authors
Tseng, R. J., Padgett, D. A., Dhabhar, F. S., Engler, H., & Sheridan, J. F.
Affiliations
  • The Ohio State University (US)
  • The Ohio State University Wexner Medical Center (US)
Corresponding author
Sheridan, John F.
ORCID
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2005-03
Volume
19
Issue
2
Pages
153-164
ISSN
0889-1591 (ISSN-L)
DOI
10.1016/j.bbi.2004.07.001
OpenAlex
W1982075489
Cited by
59
References
52
Citations by year
2024: 3 · 2023: 1 · 2022: 1 · 2021: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 2 · 2014: 2 · 2013: 5 · 2012: 5
FWCI
2.02
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5f30de005746-05)
  • National Institute of Mental Health (MH46801, R01MH046801)
  • National Institute of Allergy and Infectious Diseases (AI48995, R01AI048995)
  • National Institute of Dental and Craniofacial Research (DE05746)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
Keywords
NK cell cytotoxicity, restraint stress, glucocorticoids, opioids, mu-opioid receptor, hypothalamic-pituitary-adrenal axis, mifepristone, naltrexone, beta-funaltrexamine, innate immunity, viral infection, splenic NK cells
MeSH terms
Animals, Glucocorticoids, Hormone Antagonists, Killer Cells, Natural, Male, Mice, Inbred C57BL, Naltrexone, Narcotic Antagonists, Orthomyxoviridae Infections, Influenza A virus, Restraint, Physical, Spleen, Stress, Physiological, Neuroimmunomodulation, Mifepristone, Receptors, Opioid, mu, Receptors, Opioid, delta, Receptors, Opioid, kappa, Lymphocyte Count, Mice

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