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Infection and Immunity, August 2007, p. 3823-3832, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01335-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Cytokines, Signaling Pathways, and Effector Molecules Required for the Control of Leishmania (Viannia) braziliensis in Mice{triangledown}

F. Janaina Soares Rocha,1,{dagger} Ulrike Schleicher,1,2 Jochen Mattner,1,{ddagger} Gottfried Alber,3 and Christian Bogdan1,2*

Institute of Clinical Microbiology, Immunology and Hygiene, University Clinic of Erlangen, Erlangen, Germany,1 Department of Medical Microbiology and Hygiene, University Clinic of Freiburg, Freiburg, Germany,2 Institute of Immunology, College of Veterinary Medicine, University of Leipzig, Leipzig, Germany3

Received 20 August 2006/ Returned for modification 27 September 2006/ Accepted 24 April 2007

Cutaneous leishmaniasis is caused by protozoan parasites of the genus Leishmania. The mechanisms of pathogen control have been established primarily in the mouse model of Leishmania major infection, but they might not hold true for other Leishmania species associated with cutaneous disease. Here, we analyzed the role of cytokines, signaling components, and effector molecules in the control of New World cutaneous leishmaniasis due to L. braziliensis. Unlike L. major, L. braziliensis caused small, nonulcerative, and self-healing skin swelling in C57BL/6 mice, as well as BALB/c mice. In contrast to the results obtained for L. mexicana, mice deficient for interleukin-12 or its key signaling molecule, signal transducer and activator of transcription 4, rapidly succumbed to severe visceral leishmaniasis. Infection of tumor necrosis factor knockout mice with L. braziliensis led to progressive, nonhealing skin lesions with erosions and hemorrhagic ulcerations, but in contrast to the results with L. major, only 20 to 30% of the mice developed fatal visceral disease. As seen with L. major, mice with a deleted inducible nitric oxide synthase gene (iNOS–/–) were unable to contain L. braziliensis in the skin, whereas the control of the parasite in the spleen remained unimpaired. Unlike what happens in L. major infections, NADPH oxidase had no impact on the course of disease in L. braziliensis-infected mice. These results not only define essential components of a protective immune response to L. braziliensis but also illustrate that the requirements for the control of cutaneous leishmaniasis vary between different parasite species.

* Corresponding author. Present address: Mikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Universitätsklinikum Erlangen, Wasserturmstrasse 3-5, D-91054 Erlangen, Germany. Phone: 49-9131-852-2551. Fax: 49-9131-852-2573. E-mail: christian.bogdan{at}mikrobio.med.uni-erlangen.de

{triangledown} Published ahead of print on 21 May 2007.

Editor: W. A. Petri, Jr.

{dagger} Present address: Departamento de Medicina Tropical, Universidade Federal de Pernambuco, Rua Prof. Moraes Rego, s/n, Cidade Universitária, 50-670-420, Recife, Pernambuco, Brazil.

{ddagger} Present address: Department of Pathology, University of Chicago, 5847 South Maryland Avenue, Chicago, IL 60637.

Infection and Immunity, August 2007, p. 3823-3832, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.01335-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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