Activated macrophages destroy intracellular Leishmania major amastigotes by an L-arginine-dependent killing mechanism.
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- S J Green
- Department of Cellular Immunology, Walter Reed Army Institute of Research , Washington, D.C. 20307
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- M S Meltzer
- Department of Cellular Immunology, Walter Reed Army Institute of Research , Washington, D.C. 20307
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- J B Hibbs
- VA Medical Center, and Department of Medicine, Division of Infectious Diseases, University of Utah School of Medicine , Salt Lake City, UT 84148
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- C A Nacy
- Department of Cellular Immunology, Walter Reed Army Institute of Research , Washington, D.C. 20307
書誌事項
- 公開日
- 1990-01-01
- 権利情報
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- https://academic.oup.com/pages/standard-publication-reuse-rights
- DOI
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- 10.4049/jimmunol.144.1.278
- 公開者
- Oxford University Press (OUP)
この論文をさがす
説明
<jats:title>Abstract</jats:title> <jats:p>Macrophages infected with amastigotes of Leishmania major and treated with IFN-gamma in vitro develop potent antimicrobial activities that eliminate the intracellular parasite. This antileishmanial activity was suppressed in a dose dependent fashion by NG-monomethyl-l-arginine (NGMMLA), a competitive inhibitor of nitrite, nitrate, nitric oxide and l-citrulline synthesis from l-arginine. Excess l-arginine added to infected macrophage cultures reversed the inhibitory effects of NGMMLA. Addition of arginase to culture media inhibited intracellular killing by IFN-gamma-treated cells. Similar effects were seen with macrophages obtained from BCG-infected C3H/HeN mice. Increased levels of nitrite, an oxidative product of the l-arginine-dependent effector mechanism, was measured in cultures of infected IFN gamma-treated macrophages as well as infected BCG-activated macrophages. Nitrite production correlated with development of antileishmanial activity. Nitrite production and microbicidal activity both decreased when in vivo or in vitro-activated macrophages were cultured in the presence of either arginase or NGMMLA. Nitric oxide synthesized from a terminal guanidino nitrogen atom of l-arginine and a precursor of the nitrite measured, may disrupt Fe-dependent enzymatic pathways vital to the survival of amastigotes within macrophages.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 144 (1), 278-283, 1990-01-01
Oxford University Press (OUP)