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Acute stress transiently activates macrophages and chemokines in cervical lymph nodes

ABSTRACT: Lymph nodes are vital for optimizing immune responses. Stress can induce several cellular and humoral immune responses. Acute restraint stress (RS) is a routinely used experimental procedure for studying psychological and/or physiological stress effects. Here, we determined the impact of RS on cervical lymph nodes in rats at the molecular and cellular levels. Stress was induced in male Sprague-Dawley rats by immobilization for 30, 60, and 120 min (RS30, RS60, and RS120, respectively) relative to a no-stress control (C) group. Expression of genes encoding chemokines CXCL1/CXCL2 (Cxcl1 and Cxcl2) and their receptor CXCR2 (Cxcr2) was analyzed at the mRNA level by reverse transcription-quantitative PCR (RT-qPCR) and microarray analyses. Immunohistochemistry and in situ hybridization were performed to determine the expression of these moieties along with the macrophage biomarker, CD68. Microarray analysis revealed that expression of 514 and 496 genes was upregulated and downregulated, respectively, in RS30. Cxcl1 and Cxcl2 expression showed a 23- and 13-fold increase, respectively, in RS30 relative to the C group. Expression of Cxcr2 was upregulated by approximately 1.6-fold in RS30 relative to the C group. Gene ontology analysis of three upregulated genes induced by RS30 suggested that they may be responsible for the cytokine network, inflammation, as well as leukocyte chemotaxis and migration. RT-qPCR analysis indicated that the mRNA levels of Cxcl1 and Cxcl2 significantly increased in RS30 but reverted to normal levels in RS60 and RS120. Cxcr2 mRNA level also increased significantly in RS30 and RS120 relative to the C group. RS-induced CXCL1-immunopositive cells corresponded to B/plasma cells, while CXCL2-immunopositive cells corresponded to endothelial cells of the high endothelial venules. Stress-induced CXCR2-immunopositive cells corresponded to macrophages. Psychological and/or physiological stress induces acute stress response and immunoreactive microenvironment in cervical lymph nodes, and the CXCL1/CXCL2-CXCR2 axis is pivotal in acute stress response.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE202994 | GEO | 2024/04/24

REPOSITORIES: GEO

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Project description:[Background] TNFa-induced adipose-related protein (TIARP) is a six-transmembrane protein that is expressed on macrophages, neutrophils and synoviocytes. We have recently reported that TIARP deficient mice (TIARP-/-) spontaneously developed arthritis, and had the high susceptibility to collagen-induced arthritis (CIA) with enhanced interleukin (IL)-6 production. However, the effect of TIARP to neutrophils and fibroblast-like syonoviocytes (FLS) has not been clearly elucidated. [Methods] We analyzed the roles of TIARP in K/BxN serum transfer model using TIARP-/- mice. We characterized the differences of neutrophils between WT and TIARP-/- mice by DNA microarray. Transmigration assays of TIARP-/- neutrophils were performed in vitro and in vivo. FLS were cultured with TNF? and the production of CXCL2 (a specific ligand of CXCR1 and CXCR2) and IL-6 were measured by ELISA. Moreover, TIARP-/- mice transferred with K/BxN serum were treated with anti-IL-6R antibodies. [Results] Arthritis in TIARP-/- mice transferred with K/BxN serum was significantly exacerbated. We identified overexpression of CXCR1 and CXCR2 in TIARP-/- neutrophils by DNA microarray. Neutrophils from TIARP-/- mice showed strong migration activity. The enhancement of chomotactic activity of TIARP-/- neutrophil was greatly facilitated by CXCL2 in vitro and in vivo. In addition, TIARP-/-FLS has enhanced the production of CXCL2 and IL-6 and the cell proliferation in the presence of TNFa, and the blockade of IL-6R significantly attenuated arthritis in vivo. [Conclusion] Our findings indicate that TIARP might down-regulate the production of CXCL2 and IL-6 in FLS, and the expression of chemokine receptors (CXCR1 and CXCR2) in neutrophils, resulting in the protective ability of neutrophils migration into arthritic joints. Mice were treated with thiogycollate medium intraperitoneally. After 3 days, peritoneal macrophages were isolated from three WT or TIARP-deficient mice, and these cells were stimulated by TNF? for 24 hours. Ly6G+ Neutrophils were isolated from splenocytes by MACS.

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Acute stress transiently activates macrophages and chemokines in cervical lymph nodes

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