Abstract
BackgroundVisceral leishmaniasis (VL) is a neglected tropical disease (NTD), caused by the intracellular protozoan parasites Leishmania donovani and Leishmania infantum. Symptomatic VL is considered fatal when left untreated. At present, there is no effective vaccine licensed for human use and available chemotherapies have limitations. Understanding the local immune mechanisms required for the control of infection is a key factor for developing effective vaccines and therapeutics.MethodsWe have investigated the development of the typical granulomatous lesions in the liver in experimental VL over time, together with the local immune responses. BALB/c mice were infected intravenously with a dose of 2 × 107 L. donovani amastigotes (MHOM/ET/67/HU3) and sacrificed at 15, 35 and 63 days post-infection (dpi). Histopathology and immunohistochemical techniques were used for the detection of Leishmania antigen, selected cell types including B and T lymphocytes, macrophages and neutrophils (CD45R-B220+, CD3+, F4/80+ and Ly-6G+) and iNOS.ResultsGranulomatous lesions were identified as early as 15 dpi in the livers of all infected animals. Three categories were used to classify liver granulomas (immature, mature and clear). Clear granulomas were exclusively detected from 35 dpi onwards. Kupffer cells (F4/80+) were predominant in immature granulomas, regardless of the dpi. Nonetheless, the highest expression was found 63 dpi. Positive staining for iNOS was mainly observed in the cytoplasm of fused Kupffer cells and the highest expression observed at 35 dpi. T cells (CD3+) and B cells (CD45R-B220+) were predominant in more advanced granuloma stages, probably related to the establishment of acquired immunity. Neutrophils (Ly-6G+) were predominantly observed in mature granulomas with the highest expression at 15 dpi. Neutrophils were lower in numbers compared to other cell types, particularly at later time points.ConclusionsOur results reflect the role of macrophages during the early stage of infection and the establishment of a lymphocytic response to control the infection in more advanced stages.
Highlights
Visceral leishmaniasis (VL) is a neglected tropical disease (NTD), caused by the intracellular protozoan parasites Leishmania donovani and Leishmania infantum
VL is caused by the intracellular protozoan parasites Leishmania donovani in Asia and Africa and Leishmania infantum in Latin America and the Mediterranean region [5]
Histopathology Granulomas and aggregations of macrophages were present in the livers of all infected animals from 15 dpi onwards (Fig. 1)
Summary
Visceral leishmaniasis (VL) is a neglected tropical disease (NTD), caused by the intracellular protozoan parasites Leishmania donovani and Leishmania infantum. Leishmaniasis is one of the most prevalent parasitic public health problems worldwide [1, 2]. This term includes cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis [3] and visceral leishmaniasis (VL) [2, 4]. VL is caused by the intracellular protozoan parasites Leishmania donovani in Asia and Africa and Leishmania infantum in Latin America and the Mediterranean region [5]. In the Mediterranean basin and Latin America, VL is considered a zoonosis caused by L. infantum. Northward spread of VL endemic foci in Italy has been reported [7]
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