Concurrent depression of tumor macrophage infiltration and systemic inflammation by progressive cancer growth.
Macrophage accumulation during the growth of a peritoneal ascites and three s.c. tumors in two animal species was analyzed and correlated with the capacity of the same tumor-bearing host to respond to inflammatory stimuli at sites distant to the tumor. Two of the three s.c. tumors induced systemic defects in macrophage accumulation; the tumor that did not (P-815 mastocytoma) did depress inflammation when transplanted to the peritoneal site. Macrophage accumulation within different tumors varied but, for a given tumor, it occurred in proportion to tumor growth when systemic inflammatory reactions were normal. However, the tumor to macrophage ratio increased dramatically and concurrently with onset of the generalized defect in macrophage inflammatory responsiveness. Accordingly, we concluded that macrophage mobility tested at remote sites is indicative of inflammatory events within the tumor. However, the antiinflammatory effect directed against macrophages is probably not a significant factor in tumor emergence since the required number of tumor cells was large and variable between not only tumors but also sites of transplantation.
D000818:Animals; D002452:Cell Count; D005354:Fibrosarcoma / Q000473:pathology; D007249:Inflammation / Q000473:pathology*; D008264:Macrophages / Q000473:pathology*; D012515:Mast-Cell Sarcoma / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D009368:Neoplasm Transplantation; D051381:Rats; D011919:Rats, Inbred Strains; D012513:Sarcoma, Experimental / Q000473:pathology*; D012983:Soft Tissue Neoplasms / Q000473:pathology; D014185:Transplantation, Isogeneic