期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 293, 期 3, 页码 R1180-R1190出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00307.2007
关键词
innate immunity; Escherichia coli; social stress; psychoneuroimmunology
类别
资金
- NIDCR NIH HHS [T32 DE 014320-06] Funding Source: Medline
- NIMH NIH HHS [R01 MH 046801-15] Funding Source: Medline
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 stressinduced 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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