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*Centro de Pesquisas Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil;
Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de Santa Catarina, Florianópolis, Brazil;
Instituto de Investigação em Imunologia, Salvador, Brazil; and
Universidade Federal da Bahia, Salvador, Brazil
Neutrophils play an active role in the control of infections caused by intracellular pathogens such as Leishmania. In the present study, we investigated the effect of neutrophil depletion at the time of Leishmania braziliensis infection of BALB/c mice and how neutrophils interact with the infected macrophage to promote parasite elimination. The in vivo depletion of neutrophils led to a significant increase in parasite load and enhanced the Th1-Th2 immune response in this experimental model of infection. BALB/c mice coinoculated with both parasites and live neutrophils displayed lower parasite burdens at the site of infection and in the draining lymph nodes. In vitro, we observed that live neutrophils significantly reduced the parasite load in L. braziliensis-infected murine macrophages, an effect not observed with Leishmania major. L. braziliensis elimination was dependent on the interaction between neutrophils and macrophages and was associated with TNF-
as well as superoxide production. Furthermore, cooperation between neutrophils and macrophages toward parasite elimination was also observed in experiments performed with L. braziliensis-infected human cells and, importantly, with two other New World Leishmania species. These results indicate that neutrophils play an important and previously unappreciated role in L. braziliensis infection, favoring the induction of a protective immune response.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants from Programa Estratégico de Apoio à Pesquisa em Saúde (PAPES)/Fundação Oswaldo Cruz and Conselho Nacional de Desenvolvimento Científico e Tecnológica (CNPq). F.O.N. was supported by a Commissao de Aperfeiçoamento de Pessoal Nival Superior fellowship and R.S. and L.A. were supported by CNPq fellowships. A.Báfica, V.M.B., C.B., M.B.N., A.Barral, and C.I.O. are senior investigators from CNPq and Instituto de Investigação em Imunologia (iii).
2 Address correspondence and reprint requests to Dr. C. I. de Oliveira, Rua Waldemar Falcão, 121, Salvador, BA, Brazil, CEP 40296–710. E-mail address: camila{at}bahia fiocruz.br
3 Abbreviations used in this paper: Lb, L. braziliensis; PMN, polymorphonuclear neutrophil; NAC, N-acetylcysteine; dLN, draining lymph node; WT, wild type.
4 The online version of this article contains supplemental material.
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