Abstract
Visceral leishmaniasis is a neglected disease caused by Leishmania protozoa parasites transmitted by infected sand fly vectors. This disease represents the second in mortality among tropical infections and is associated to a profound immunosuppression state of the host. The hallmark of this infection-induced host immunodeviation is the characteristic high levels of the regulatory interleukin-10 (IL-10) cytokine. In the present study, we investigated the role of B-1 cells in the maintenance of splenic IL-10 levels that could interfere with resistance to parasite infection. Using an experimental murine infection model with Leishmania (L.) infantum chagasi we demonstrated an improved resistance of B-1 deficient BALB/XID mice to infection. BALB/XID mice developed a reduced splenomegaly with diminished splenic parasite burden and lower levels of IL-10 secretion of purified splenocytes at 30 days post-infection, as compared to BALB/c wild-type control mice. Interestingly, we found that resident peritoneal macrophages isolated from BALB/XID mice were more effective to control the parasite load in comparison to cells isolated from BALB/c wild-type mice. Our findings point to a role of B-1 cells in the host susceptibility to visceral leishmaniasis.
Highlights
Visceral leishmaniasis (VL), known as Kala Azar is a neglected tropical disease caused by the intracellular protozoan Leishmania donovani and Leishmania (L.) infantum chagasi parasites (Kaye and Scott, 2011)
The initial steps of a immune response against Leishmania infection is triggered from the activation of innate receptors pattern recognition receptors (PRRs) by molecules associated with pathogens (MMAPs) such as lipophosphoglycans, glycoinositolphospholipid, and metalloproteinase GP63, all expressed on parasite cell surface (Liu and Uzonna, 2012)
We used a murine model of VL in which infection of BALB/c mice with L. (L.) infantum chagasi amastigotes gives rise to a higher parasite load in the first weeks of infection, after which it is controlled by the host immune response
Summary
Visceral leishmaniasis (VL), known as Kala Azar is a neglected tropical disease caused by the intracellular protozoan Leishmania donovani and Leishmania (L.) infantum chagasi parasites (Kaye and Scott, 2011). Over 90% of the annual incidence of new cases occurs in Bangladesh, India, Nepal, Sudan, South Sudan, Ethiopia, and Brazil In these countries, the outbreaks and prevalence of infection, from which are reported clinical cases, differ in their eco-epidemiology and sand fly vectors involved. The initial steps of a immune response against Leishmania infection is triggered from the activation of innate receptors pattern recognition receptors (PRRs) by molecules associated with pathogens (MMAPs) such as lipophosphoglycans, glycoinositolphospholipid, and metalloproteinase GP63, all expressed on parasite cell surface (Liu and Uzonna, 2012). Macrophages are able to secrete reactive oxygen species (ROS) and nitric oxide (NO), both involved in the destruction of parasites (Kaye and Scott, 2011; Liu and Uzonna, 2012)
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