Macrophages participate in host protection and the disease pathology associated with Leishmania braziliensis infection
1 Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Bahia, Brazil
2 Instituto Nacional de Ciência e Tecnologia de Doenças Tropicais- INCT-DT(CNPq/MCT), Salvador, Bahia, Brazil
3 Complexo Hospitalar Universitário Prof. Edgard Santos, Serviço de Imunologia, 5o andar, Rua João das Botas, s/n, Canela, 40110-160 Salvador, BA, Brazil
BMC Infectious Diseases 2012, 12:75 doi:10.1186/1471-2334-12-75Published: 29 March 2012
Leishmania preferentially infects macrophages, which allow the parasite to multiply but can also kill the parasite. Although the T cell response in human leishmaniasis is well-characterized, little is known about the concomitant macrophage behavior. The aim of this study was to characterize the macrophage immune response after Leishmania braziliensis infection in cells derived from cutaneous leishmaniasis (CL) or mucosal leishmaniasis (ML) patients, subclinical individuals (SC) and healthy control subjects (HS).
Peripheral blood mononuclear cell-derived macrophages from the different groups were exposed to L. braziliensis in vitro and were evaluated for susceptibility to Leishmania infection, ability to kill Leishmania and chemokine/cytokine production. Nitric Oxide (NO) and superoxide (O2-) levels in the supernatant of infected macrophage cultures were monitored.
After exposure to L. braziliensis, peripheral blood mononuclear cell-derived macrophages from SC individuals showed a lower infection rate and a smaller number of intracellular amastigotes compared to cells from CL and ML patients. Macrophages from CL and ML patients produced more chemokines and TNF-α than those from the SC group. Production of NO and O2- were detected but did not vary significantly among the different groups.
Our data indicate that macrophages play a pivotal role in controlling L. braziliensis infection and in leishmaniasis pathology by secreting pro-inflammatory chemokines/cytokines that activate and recruit T cells, overwhelming the inflammatory response.