IN-VIVO MACROPHAGE FUNCTION IN EXPERIMENTAL-INFECTION WITH TRYPANOSOMA-CRUZI SUBPOPULATIONS

Citation
Am. Celentano et Smg. Cappa, IN-VIVO MACROPHAGE FUNCTION IN EXPERIMENTAL-INFECTION WITH TRYPANOSOMA-CRUZI SUBPOPULATIONS, Acta Tropica, 55(3), 1993, pp. 171-180
Citations number
39
Categorie Soggetti
Biology,"Tropical Medicine",Parasitiology
Journal title
ISSN journal
0001706X
Volume
55
Issue
3
Year of publication
1993
Pages
171 - 180
Database
ISI
SICI code
0001-706X(1993)55:3<171:IMFIEW>2.0.ZU;2-5
Abstract
The macrophage function was investigated in mice infected with Trypano soma cruzi. Two subpopulations of the parasite were utilized, RA and K 98. Strain RA is efficiently internalized by macrophages and is lethal for mice, and clone K98 is poorly phagocytosed by macrophages and is not lethal. Treatment with silica enhanced parasitemia and mortality i n mice infected with both parasite subpopulations. Parasitemia kinetic s, however, were affected only in mice infected with RA, which suggest s that macrophage effector mechanisms may play a more relevant role in this experimental group than in mice infected with K98. Resistance to Salmonella typhimurium infection and bactericidal activity of macroph ages depended upon the T. cruzi subpopulation utilized and the infecti on period. Infection with K98 induced only a trend towards enhanced re sistance to bacterial challenge during both the acute and chronic phas es, whereas a significantly enhanced bactericidal activity of spleen a nd liver phagocytes was observed. Mice acutely infected with RA showed significantly enhanced susceptibility to S. typhimurium infection and lower bactericidal activity. Mice surviving infection with this aggre ssive strain, however, showed significantly enhanced resistance and ba ctericidal activities. Mice acutely infected with the RA strain displa yed a dissociation between macrophage capacities to control S. typhimu rium and T. cruzi. A similar phenomenon was also observed in other par asitoses (schistosomiasis, African trypanosomiasis). This fact may be due to differences in the lethal mechanisms through which macrophages control these parasites and S. typhimurium.