Inhibition of in vivo neutrophil accumulation by stress. Possible role of neutrophil adherence.

Psychological stress results in neural and endocrine changes which can alter various aspects of the immune system. However, the effects of stress on inflammation has not received much attention despite the fact that stress hormones, such as the corticosteroids, are known to reduce inflammation. The present study extends a previous finding that stress itself can reduce inflammation. In the first experiment, zymosan was injected into an air pouch on the dorsum of F344 rats. Half of these rats then received three hours of inescapable, intermittent, electric foot shock as a stressor. The other half of the injected rats served as nonstressed controls. A third group were given air pouches but no zymosan. Fewer neutrophils accumulated at the inflammatory site of stressed rats as compared to nonstressed control rats. However, phagocytosis of zymosan by air pouch neutrophils was higher in stressed rats. Peripheral perfusion was not altered significantly by shock, but vascular permeability was reduced in stressed rats. The effects of stress on peripheral blood leukocytes of rats not injected with zymosan was investigated. It was found that while peripheral blood monocytes and lymphocyte numbers were decreased by stress, neutrophils were not decreased. Increased neutrophil adherence was found in stressed rats. Additionally, in the presence of endotoxin, neutrophils from stressed rats did not increase their adherence as much as those of control rats. The increased adhesiveness of neutrophils in stressed animals may account for the diminished inflammatory response in the shocked rats.