Immunological profile of resistance and susceptibility in naturally infected dogs by Leishmania infantum

- We performed a detailed investigation to identify immunobiomarkers of resistance and susceptibility in naturally infected dogs by Leishmania infantum.
- Symptomatic dogs display lower circulating T and B lymphocytes with higher production of IFN-γ and IL-4 whereas asymptomatic dogs-I exhibit a cellular immunoprofile similar with healthy animals during CVL.
- The animals with asymptomatic (AD-II) and symptomatic (SD) clinical forms exhibited a mixed (Th1/Th2) immune profile.

Visceral leishmaniasis has a great impact on public health, and dogs are considered the main domestic reservoir of Leishmania infantum, the causal parasite. In this study, 159 animals naturally infected by L. infantum from an endemic area of Brazil were evaluated through an analysis of cellular responses, using flow cytometry, and of the hematological parameters. The results confirmed that disease progression is associated with anemia and reductions in eosinophils, monocytes and lymphocytes. The investigation of the immune response, based on the immunophenotypic profile of peripheral blood, showed declines in the absolute numbers of T lymphocytes CD5+ and their subsets (CD4+ and CD8+) and a drop of B lymphocytes in asymptomatic seropositive (AD-II) and symptomatic seropositive (SD) dogs. Neutrophils, when stimulated with soluble antigen of L. infantum, showed higher synthesis of interferon (IFN)-γ+ in AD-II and SD groups, with decreased production of interleukin (IL)-4+ in asymptomatic seronegative dogs positive for L. infantum infection based on polymerase chain reaction testing (AD-I group). In the AD-II and SD groups, subpopulations of stimulated lymphocytes (CD4+ and CD8+) also exhibited greater synthesis of IFN-γ+ and IL-4+ in culture. These results suggest that the animals of the AD-II and SD groups exhibited a mixed immune response (Type 1 and 2) and the AD-I group presenting an immune profile very similar to normal control animals.