Early infection with Leishmania major restrains pathogenic response to Leishmania amazonensis and parasite growth.

• Autor(a) principal: Lombana, Claudia Zuleida Gonzalez
• Data de Publicação: 2008
• Outros Autores: Santiago, Helton da Costa, Macedo, J. P., Rego, Virgínia Aparecida Seixas, Russo, Remo de Castro, Tafuri, Wagner Luiz, Afonso, Luís Carlos Crocco, Vieira, Leda Quercia
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFOP
• Texto Completo: http://www.repositorio.ufop.br/handle/123456789/4613; https://doi.org/10.1016/j.actatropica.2007.12.012
• topic: Protozoan parasites; Cutaneous leishmaniasis; Infection; Cellular recruitment

Experimental models of infection with Leishmania spp. have provided knowledge of several immunological events involved in the resistance mechanism used by the host to restrain parasite growth. It is well accepted that concomitant immunity exists, and there is some evidence that it would play a major role in long-lasting acquired resistance to infection. In this paper, the resistance to Leishmania amazonensis infection in C57BL/6 mice infected with Leishmania major was investigated. C57BL/6 mice, which spontaneously heal lesions caused by infection with L. major, were infected with L. amazonensis at different times before and after L. major. We demonstrated that C57BL/6 mice previously infected with L. major restrain pathogenic responses induced by L. amazonensis infection and decrease parasite burdens by one order of magnitude. Coinfected mice showed production of IFN-_ in lesions similar to mice infected solely with L. major, but higher TNF-_ and nitric oxide synthase (iNOS) mRNA expression was observed. Surprisingly, the restrained pathogenic response was not related to IL-10 production, as evidenced by lower levels of both mRNA, protein expression in lesions from co-infected mice and in co-infections in IL-10−/− mice. Examination of the inflammatory infiltrate at the site of infection showed a reduced number of monocytes and lymphocytes in L. amazonensis lesions. Additionally, differential production of the CCL3/MIP-1_ and CCL5/RANTES was observed. We suggest that the control of lesion progression caused by L. amazonensis in C57BL/6 mice pre-infected with L. major is related to the induction of a down-regulatory environment at the site of infection with L. amazonensis.