Leishmania spp. promastigotes preferentially infect host macrophages, where parasite internalization is facilitated by several host and parasite surface molecules. This study aimed to demonstrate the role of humoral immunity in Leishmania parasite internalization into host macrophages. First, informed consent sera were obtained from 67 parasitologically confirmed visceral leishmaniasis patients reporting to our field treatment centre, Eastern Sudan. Then following titre determination, sera that had a titre of >102,400 were selected for parasite coating. An in vitro parasite internalization system was developed to enhance the Leishmania/ macrophage interactions. The mean parasite number per monocytes was 626 ± 91 for antibody-coated Leishmania donovani, compared to 412 ± 70 uncoated isolates (p= 0.01). On the other hand, the percentage of infected cells was significantly higher for all antibody-coated isolates (100%) compared to uncoated ones (40%). This evidence of high infectivity probably points to the fact that anti-Leishmania antibodies facilitated the parasite uptake by host macrophages and monocytes-derived macrophages (MDM). Moreover, the rate of parasite uptake by MDM was significantly higher compared to monocytes (p= 0.00). This could be explained by the fact that the functional capabilities of fully differentiated macrophages differ from monocytes. In conclusion, host humoral immunity probably plays a pivotal role in Leishmania parasites internalization into host macrophages.
Key words: Leishmania donovani, macrophages, monocyte-derived macrophages, humoral immunity
DAT, Direct agglutination test; SSG, sodium stibogluconate; MDMs, monocyte-derived macrophages; PBMCs, peripheral blood monocytes; NNN, Novy-Macneal-Nicolle; PBS, phosphate buffered saline; RPMI, Rosuell Park Memorial Institute; FCS, foetal calf serum; EDTA, ethylenediaminetetraacetic acid; PKDL, post-kala-azar dermal leishmaniasis
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