title: Acute cold stress induces suppressor macrophages in mice.
abstract: To elucidate mechanisms underlying acute cold stress-induced immunosuppression, functions of murine peritoneal cells of monocyte/ macrophage lineage from acute cold-stressed mice (exposed to 5 degrees C for 24 h) were investigated. Proliferative responses of spleen cells from control mice (reared at 25 degrees C) stimulated with concanavalin A (ConA) were significantly suppressed by adding peritoneal exudate cells from mice immediately after acute cold stress. The proportion of adherent cells was markedly increased in the peritoneal exudate cells from acute cold-stressed mice. These adherent cells from acute cold-stressed mice were shown to be the cells responsible for the suppressor activity for ConA responses of control spleen cells. Nonadherent cells did not suppress the ConA responses. The adherent cells in peritoneal exudate cells from control mice also suppressed the ConA responses, the inhibitory effect being considerably lower than that from acute cold-stressed mice. Addition of a nitric oxide synthase substrate analogue, NG-monomethyl-L-arginine, to the mixed cell cultures of normal spleen cells and adherent cells from acute cold-stressed mice inhibited nitric oxide release and completely abolished the suppressive effect of the adherent cells, suggesting that reactive nitrogen oxide released from the activated macrophages is apparently involved in the downregulation of proliferative responses of T cells. Thus the present findings suggest that acute cold stress induces macrophages with suppressor function and that this may contribute to the immune-suppressive state seen in spleen cells from acute cold-stressed mice.
authors.affiliation: Department of Hygiene, National Defense Medical College, Tokorozawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kizaki
authors.forename: S
authors.initials: S
authors.lastname: Oh-ishi
authors.forename: H
authors.initials: H
authors.lastname: Ohno
mesh_terms: D000208:Acute Disease; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000502:physiology; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects / Q000502:physiology; D002448:Cell Adhesion / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D003080:Cold Temperature / Q000009:adverse effects*; D003208:Concanavalin A / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005122:Exudates and Transudates / Q000166:cytology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000502:physiology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008934:Mitogens / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D013154:Spleen / Q000166:cytology / Q000187:drug effects; D013312:Stress, Physiological / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D008934:Mitogens; D003208:Concanavalin A; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase