Title : Roles of endogenous gamma interferon and macrophage microbicidal mechanisms in host response to chemotherapy in experimental visceral leishmaniasis.

Pub. Date : 2000 Jan

PMID : 10603400






5 Functional Relationships(s)
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1 Sb was active (>94% killing), however, in both inducible nitric oxide synthase (iNOS) knockout (KO) and respiratory burst (phagocyte oxidase)-deficient chronic granulomatous disease (X-CGD) mice. Antimony nitric oxide synthase 2, inducible Mus musculus
2 Sb was active (>94% killing), however, in both inducible nitric oxide synthase (iNOS) knockout (KO) and respiratory burst (phagocyte oxidase)-deficient chronic granulomatous disease (X-CGD) mice. Antimony nitric oxide synthase 2, inducible Mus musculus
3 Sb"s efficacy was also maintained in doubly deficient animals (X-CGD mice treated with an iNOS inhibitor). Antimony nitric oxide synthase 2, inducible Mus musculus
4 Although resolution of L. donovani infection requires iNOS, residual visceral infection remained largely suppressed in iNOS KO mice treated with Sb or AmB. Antimony nitric oxide synthase 2, inducible Mus musculus
5 Treatment with either Sb or AmB permits an iNOS-independent mechanism to emerge and control residual intracellular L. donovani infection. Antimony nitric oxide synthase 2, inducible Mus musculus