Acute cold stress induces suppressor macrophages in mice.
Kizaki, Takako, Shuji Oh-Ishi, and Hideki Ohno.
Department of Hygiene, National Defense Medical College, Tokorozawa
359, Japan
APStracts 3:0144A, 1996.
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 C for 24 h) were investigated. Proliferative responses of spleen
cells from control mice (reared at 25 C) stimulated with Concanavalin
A (Con A) 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 Con A responses of control spleen cells. Non
-adherent cells did not suppress the Con A responses. The adherent
cells in peritoneal exudate cells from control mice also suppressed
the Con A responses, the inhibitory effect being considerably lower
than that from acute cold-stressed mice. Addition of a nitric oxide
(NO) 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 NO 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 down-regulation 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.
Received 28 December 1995; accepted in final form 14 February
1996.
APS Manuscript Number A1353-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96