Responses to Leishmania donovani in mice deficient in both phagocyte oxidase and inducible nitric oxide synthase.
Mice deficient in phagocyte oxidase (phox) and inducible nitric oxide synthase (iNOS), which are primary macrophage killing mechanisms, generated tissue granulomas but showed unrestrained Leishmania donovani visceral replication and suboptimal initial responsiveness to antimony treatment. Nevertheless, visceral infection was controlled post-treatment and did not recur. A phox/iNOS-independent macrophage mechanism, which was not triggered by L. donovani, emerges after chemotherapy.
Murray
Henry W
HW
Department of Medicine, Weill Medical College of Cornell University, New York, New York 10021, USA. hwmurray@med.cornell.edu
Xiang
Zhaoying
Z
Ma
Xiaojing
X
D000666:Amphotericin B / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D000967:Antimony Sodium Gluconate / Q000008:administration & dosage / Q000494:pharmacology; D000981:Antiprotozoal Agents / Q000008:administration & dosage / Q000494:pharmacology; D020558:GTP Phosphohydrolases / Q000096:biosynthesis; D020869:Gene Expression Profiling; D015745:Granuloma, Foreign-Body / Q000469:parasitology; D007893:Leishmania donovani / Q000187:drug effects / Q000276:immunology*; D007898:Leishmaniasis, Visceral / Q000188:drug therapy / Q000276:immunology* / Q000469:parasitology; D008099:Liver / Q000469:parasitology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D052247:Nitric Oxide Synthase Type II / Q000172:deficiency / Q000378:metabolism*; D010088:Oxidoreductases / Q000172:deficiency / Q000378:metabolism*; D010586:Phagocytes / Q000201:enzymology* / Q000276:immunology; D013154:Spleen / Q000469:parasitology
D000981:Antiprotozoal Agents; D000666:Amphotericin B; D010088:Oxidoreductases; D052247:Nitric Oxide Synthase Type II; D020558:GTP Phosphohydrolases; D000967:Antimony Sodium Gluconate