Stress-induced enhancement of leukocyte trafficking into sites of surgery or immune activation

Abstract

Effective immunoprotection requires rapid recruitment of leukocytes into sites of surgery, wounding, infection, or vaccination. In contrast to immunosuppressive chronic stressors, short-term acute stressors have immunoenhancing effects. Here, we quantify leukocyte infiltration within a surgical sponge to elucidate the kinetics, magnitude, subpopulation, and chemoattractant specificity of an acute stress-induced increase in leukocyte trafficking to a site of immune activation. Mice acutely stressed before sponge implantation showed 200 -300% higher neutrophil, macrophage, natural killer cell, and T cell infiltration than did nonstressed animals. We also quantified the effects of acute stress on lymphotactin-(LTN; a predominantly lymphocyte-specific chemokine), and TNF-␣-(a proinflammatory cytokine) stimulated leukocyte infiltration. An additional stress-induced increase in infiltration was observed for neutrophils, in response to TNF-␣, macrophages, in response to TNF-␣ and LTN, and natural killer cells and T cells in response to LTN. These results show that acute stress initially increases trafficking of all major leukocyte subpopulations to a site of immune activation. Tissue damage-, antigen-, or pathogen-driven chemoattractants subsequently determine which subpopulations are recruited more vigorously. Such stress-induced increases in leukocyte trafficking may enhance immunoprotection during surgery, vaccination, or infection, but may also exacerbate immunopathology during inflammatory (cardiovascular disease or gingivitis) or autoimmune (psoriasis, arthritis, or multiple sclerosis) diseases.chemokine ͉ psychophysiological stress ͉ surgical sponge ͉ wound healing ͉ lymphotactin

Pregnancy-Associated Exosomes and Their Modulation of T Cell Signaling

“…Regulatory T cells expressing CTLA-4 can induce dendritic cells to express indoleamine 2,3-dioxygenase (IDO) by interacting with its ligand CD80-CD86, thereby promoting maternal tolerance of the fetal allograft (47). Regardless of lymphoid cell number, pregnancy-associated immunosuppression has been linked with impaired IL-15 signaling, which uses the intermediate, JAK3 (48). Failure to generate an effective regulatory T cell can result in the loss or absence of maternal tolerance, potentially leading to pregnancy loss (47).…”

Behavioral Activities, Physiological Body Reactions, Hematological Parameters and Hormonal Profiles for Bucks of New Zealand White and Baladi Red Rabbits Exposed to Short Term of High Temperature

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An inflammatory review of glucocorticoid actions in the CNS

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