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Cited by 124Immune Response and InflammationStress Responses and CortisolCancer, Stress, Anesthesia, and Immune Response

Repeated social defeat increases the bactericidal activity of splenic macrophages through a Toll-like receptor-dependent pathway

Bailey, Michael T., Engler, Harald, Powell, Nicole D., Padgett, David A., Sheridan, John F.·2007·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
DOI 10.1152/ajpregu.00307.2007
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Abstract

Phagocytes of the innate immune system, such as monocytes/macrophages, represent a first line of defense against invading microorganisms. Psychological stress is often thought to suppress the functioning of these cells, in part due to the immunosuppressive activity of stress-induced glucocorticoid hormones. However, exposure to the stressor social disruption (SDR) has been shown to increase cytokine production by monocytes/macrophages and to reduce their sensitivity to corticosterone. Thus, it was hypothesized that splenic monocytes/macrophages from socially stressed mice would be primed to be more physiologically active than cells from nonstressed controls. Flow cytometry was used to demonstrate that exposure to SDR significantly increased the expression of Toll-like receptors (TLR) 2 and 4 on the surface of splenic macrophages. In a follow-up experiment, exposure to SDR also increased the ability of these macrophages to kill Escherichia coli ex vivo and in vivo. However, SDR failed to increase the bactericidal activity of splenic macrophages from C3H/HeJ mice, which lack functional TLR4. In mice with functional TLR4, the stress-induced increase in bactericidal activity was associated with a significant increase in macrophage gene expression for inducible nitric oxide synthase and subunits of the NADPH oxidase complex, which are responsible for generating reactive nitrogen and oxygen intermediates, respectively. This stress-induced increase in gene expression was not evident in the TLR4-deficient mice. These data indicate that SDR increases TLR expression, which in turn enhances the bactericidal activity of splenic macrophages, in part by increasing pathways responsible for reactive oxygen and nitrogen intermediate production.

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  • These cells are termed 'primed' because they produce enhanced proinflammatory signaling molecules and bactericidal activity when stimulated with an immune challenge.

    “These cells are termed 'primed' because they produce enhanced proinflammatory signaling molecules and bactericidal activity when stimulated with an immune challenge (Bailey et al, 2007;Powell et al, 2009).”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Bailey et al, 2007

  • Newly differentiated Ly6c hi monocytes express surface activation markers that enhance immune function, including TLRs, CCR2, and co-stimulator receptors, which are upregulated by RSD.

    “For example, surface activation markers including Toll-like receptors (TLRs), chemotactic receptors including CCR2, and co-stimulator receptors are upregulated by RSD (Avitsur et al, 2003;Engler et al, 2004;Bailey et al, 2007;Powell et al, 2009;Hanke et al, 2012).”

    From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Bailey et al, 2007

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Authors
Bailey, M. T., Engler, H., Powell, N. D., Padgett, D. A., & Sheridan, J. F.
Affiliations
The Ohio State University (US)
ORCID
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher
American Physiological Society
Published
2007-09
Volume
293
Issue
3
Pages
R1180-R1190
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
DOI
10.1152/ajpregu.00307.2007
OpenAlex
W2122309805
Cited by
124
References
59
Citations by year
2025: 2 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 5 · 2020: 5 · 2019: 5 · 2018: 4 · 2017: 6 · 2016: 10 · 2015: 8 · 2014: 5 · 2013: 10 · 2012: 16
FWCI
2.35
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (R01MH046801)
  • National Institute of Dental and Craniofacial Research (T32DE014320)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
social defeat, social stress, splenic macrophages, TLR4, TLR2, bactericidal activity, innate immunity, Escherichia coli, inducible nitric oxide synthase, NADPH oxidase, reactive oxygen species, reactive nitrogen intermediates, glucocorticoid resistance, C3H/HeJ mice, psychological stress
MeSH terms
Animals, Dominance-Subordination, Escherichia coli, Escherichia coli Infections, Flow Cytometry, Macrophages, Mice, Inbred C3H, Organ Size, Phagocytosis, Spleen, Stress, Psychological, Signal Transduction, NADPH Oxidases, Reverse Transcriptase Polymerase Chain Reaction, CD11b Antigen, Toll-Like Receptors, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, Nitric Oxide Synthase Type II

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