Article
Differential properties of CBA/J mononuclear phagocytes recovered from an inflammatory site and probed with two different species of Leishmania
Registro en:
GOMES, I. N. et al. Differential properties of CBA/J mononuclear phagocytes recovered from an inflammatory site and probed with two different species of Leishmania. Microbes and Infection, v. 5, n. 4, p. 251-260, 2003.
1286-4579
10.1016/S1286-4579(03)00025-X
Autor
Gomes, Ivana Nunes
Calabrich, Aknar Freire de Carvalho
Tavares, Rafael da Silva
Wietzerbin, Jeanne
Freitas, Luiz Antonio Rodrigues de
Veras, Patrícia Sampaio Tavares
Resumen
While CBA/J mice fail to be permissive to Leishmania amazonensis-driven pathogenic processes, they heal easily following Leishmania
major infection. The early-phase events are crucial to the outcome of Leishmania infection and it is known that macrophages (Mφ) are
important in infection control. In the present study we investigated the role of Mφ in driving CBA/J susceptibility to L. amazonensis. We
performed kinetic studies and compared the capacity of L. amazonensis and L. major to infect Mφ. There was no difference in percentages of
infection or parasite burden for 6 h between the two groups. In contrast, after 12 h we observed that infection was about twice as high in L.
amazonensis- than in L. major-infectedMφ. In addition, rIFN-c added to the cultures induced nitric oxide (NO) production, and did not modify
L. amazonensis infection, although the percentage of L. major infection was significantly reduced. This reduction in L. major infection is a
TNF-a dependent mechanism as L. major-infected Mφ expressed twice as much TNF-a mRNA as L. amazonensis-infected cells, and
anti-TNF-a reversed the IFN-c effect. Moreover, rTNF-a plus IFN-c were able to significantly reduce the percentage of L. amazonensisinfected
cells but not to the same extent as in L. major infection. Despite having higher NO production than IFN-c-treated cells,AMGaddition
to IFN-c-plus TNF-a-treated cells only partially reversed the inhibition in L. major, but not in L. amazonensis infection. Thus, in this study,
we demonstrated that L. amazonensis both inactivated and resisted innate and IFN-c-induced Mφ killing mechanisms, indicating that the
nature of the parasite and its interaction with Mφ could determine immune response polarization.