Modifications of host defence mechanisms by an acute non-immunological inflammatory reaction

Mice developing an acute non-immunological inflammatory reaction were examined for modification of specific and non-specific defence mechanisms on the basis of previous observations that these animals displayed an increased resistance to bacterial and parasitic infections but an impaired resistance to neoplasia. Local acute inflammation was induced by injection into the pleural cavity of a non-antigenic, endotoxin-free irritant--calcium pyrophosphate microcrystals or low-molecular-weight dextran. Effector functions of macrophages at remote sites from the inflammatory focus were markedly stimulated. This was shown by: (a) an accelerated elimination of Listeria monocytogenes in the liver and spleen of mice with inflammation; (b) the acquisition of cytostatic activity for tumour cells by peritoneal macrophages; and (c) an enhancement of chemiluminescence emission and superoxide production in response to phagocytosis. Natural killer activity of spleen and peritoneal cells was stimulated in a biphasic manner. In contrast, cytolytic T cell differentiation upon in vitro immunization of spleen cells against allogeneic tumour cells was impaired. All these effects were observed very early (2 h) after the onset of inflammation and were still detectable at least 3 days after the inflammatory process had disappeared.