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Organ‐specific and stage‐dependent control of Leishmania major infection by inducible nitric oxide synthase and phagocyte NADPH oxidase

Organ‐specific and stage‐dependent control of Leishmania major infection by inducible nitric... In the Leishmania major mouse model of cutaneous leishmaniasis inducible nitric oxide synthase (iNOS) is crucial for the killing of the parasite in the skin and draining lymph node. However, the effector mechanism operating against L. major in the spleen is unknown. As reactive oxygen intermediates might play a role, we analyzed macrophages and mice lacking the gp91phoxsubunit of the phagocyte NADPH oxidase (phox) for their ability to combat an infection with L. major. Macrophages from wild‐type and gp91phox–/– mice had an equal capacity to killL. major after activation by cytokines. Unlike iNOS, the activity of phox was dispensable for the resolution of the acute skin lesions and exerted only a limited effect on the containment of the parasites in the draining lymph node, but was essential for the clearance of L. major in the spleen. During the chronic phase of infection, parasites persisted at high levels in gp91phox–/– mice, and cutaneous lesions re‐emerged in approximately 60% of these mice. gp91phox deficiency did not impair the expression of iNOS or the production of TNF and IFN‐γ. These results demonstrate that iNOS and phox are both required for the control of L. major in vivo and display unexpected organ‐ and stage‐specific anti‐leishmanial effects. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Immunology Wiley

Organ‐specific and stage‐dependent control of Leishmania major infection by inducible nitric oxide synthase and phagocyte NADPH oxidase

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References (53)

Publisher
Wiley
Copyright
© 2002 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
ISSN
0014-2980
eISSN
1521-4141
DOI
10.1002/eji.200323825
pmid
12731047
Publisher site
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Abstract

In the Leishmania major mouse model of cutaneous leishmaniasis inducible nitric oxide synthase (iNOS) is crucial for the killing of the parasite in the skin and draining lymph node. However, the effector mechanism operating against L. major in the spleen is unknown. As reactive oxygen intermediates might play a role, we analyzed macrophages and mice lacking the gp91phoxsubunit of the phagocyte NADPH oxidase (phox) for their ability to combat an infection with L. major. Macrophages from wild‐type and gp91phox–/– mice had an equal capacity to killL. major after activation by cytokines. Unlike iNOS, the activity of phox was dispensable for the resolution of the acute skin lesions and exerted only a limited effect on the containment of the parasites in the draining lymph node, but was essential for the clearance of L. major in the spleen. During the chronic phase of infection, parasites persisted at high levels in gp91phox–/– mice, and cutaneous lesions re‐emerged in approximately 60% of these mice. gp91phox deficiency did not impair the expression of iNOS or the production of TNF and IFN‐γ. These results demonstrate that iNOS and phox are both required for the control of L. major in vivo and display unexpected organ‐ and stage‐specific anti‐leishmanial effects.

Journal

European Journal of Immunology – Wiley

Published: May 1, 2003

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