Cell-specific defect in monocyte function during tumor growth.

Inbred DA rats bearing a syngeneic 7,12-dimethylbenz[a]anthracene-induced neoplasm had an early impairment of chronic inflammation as measured by the numbers of monocytes elicited in a 3-day peritoneal exudative response to a sterile peptone injection. Furthermore, an advanced malignant tumor was associated with a complete block in the rats' capacity to mobilize monocytes, despite the fact that white blood cell counts on peripheral blood showed increased numbers of monocytes and polymorphonuclear leukocytes (PMN) during tumor growth. In contrast to the defect in chronic inflammation, a normal or increased acute inflammatory reponse was observed during tumor growth as measured by the 9-hour peritoneal PMN response to a sodium caseinate injection. Quantitative chemotaxis measurements in vitro made with these same peritoneal exudate cells revealed severe impairment of marcophage chemotaxis but normal migration of PMN. Generation of macrophage chemotactic signals from blood of rats with advanced tumors was not impaired. Since the resident cells of the peritoneal cavity were, chemotactically, a poor-responding population, this defective response in vitro appeared to correlate with the cell defect observed in vivo in the monocyte inflammatory response to peptone.