Stress modulates acute inflammation triggered by mycobacteria in autoimmunity-prone and normal mice.

We have investigated the effect of a single stress treatment of mice on the early cellular response (granulocyte influx) of acute inflammation that was produced by intraperitoneal inoculation of the animals with mycobacteria (10(6) bacilli of M. avium). Autoimmunity-prone (NZB/W) and normal (BALB/c, MRL, NZW) mice were submitted to the same stress (20 min of swimming) this given either before or simultaneously with the induction of the intraperitoneal mycobacteria-induced inflammation. Local inflammation was evaluated by the quantification of leukocytes harvested from the peritoneal cavity of the mice; this was done 30 and 60 minutes after the end of the stress treatment. We found that the stressor alone was able to increase the number of cells that were harvested from the peritoneal cavity; this may be due to stress-induced detachment of resident macrophages from the peritoneal walls. The autoimmunity-prone mice (NZB/W) showed a marked decrease in the number of inflammatory cells (mostly of granulocytes) when stress treatment was performed immediately before the triggering of inflammation; these stress-induced alterations were attenuated in normal mice (BALB/c and MRL strains), as well as in the non-autoimmune parent strain (NSW) of NZB/W mice. Modulation of the acute inflammatory response by stress was smaller if the stress was induced concomitantly with the triggering of inflammation; here, NZB/W were again the mice most affected by stress. Our data indicate that [1] stress is able to modify the acute inflammatory response of mice; [2] autoimmunity-prone mice are more sensitive to stress-induced modulation of inflammation than normal animals; and [3] the timing of stress (with regard to the initiation of inflammatory phenomena) is an important factor in the intensity of changes produced by stress in the early cellular response of acute inflammation.