Abstract
Sodium antimonials are one of the major and common drugs used against visceral form leishmaniasis (VL). However, the development of drug resistance makes it difficult to manage this disease. Current work investigates the modulation of splenic B cells during experimental infection with antimony-sensitive and -resistant Leishmania donovani infection. Here we phenotypically characterized splenic B cell subsets in BALB/c mice infected with antimony drug-sensitive and -resistant VL strains using flow-cytometry method. In the splenocytes we noticed increased number of Transitional T3 B cells and B1a B cells in drug-resistant VL strain infection. Besides, we also observed alteration in Follicular B cell population of antimony-resistant strain infected mice. Drug-resistant strain induced secretion of elevated level of IL-10 from B1a B cells and IL-6 from Transitional T3 B cell subsets in the splenocytes. Purified splenic B cells from antimony drug-resistant strain infected mice showed decrease in the Lyn kinase gene expression compared to sensitive strain infected and uninfected mice. The current study provides insight into changes in host splenic B-cell subsets during experimental infection with antimony-sensitive and -resistant L. donovani in murine model.
Highlights
Leishmaniases, caused by the group of parasites belonging to the genus Leishmania, have different clinical manifestations like cutaneous, mucocutaneous and visceral forms
To identify whether drugresistant strains induce higher level of IL-10 secretion from B cells, Magnetic Associated Cell Sorter purified (MACS) purified CD19+ B cells (Figure S1) from spleen of uninfected control mice were cultured and incubated for 24 h with the promastigotes of four different Leishmania strains at the ratio of 1:10 of B cell: promastigotes
Using ELISA, we observed that B cells following interaction with promastigotes of BHU575 and BHU138, antimony-resistant strains, secreted increased level of IL -10 compared to AG83 and BPK206, antimony-susceptible strains (Figure 1A)
Summary
Leishmaniases, caused by the group of parasites belonging to the genus Leishmania, have different clinical manifestations like cutaneous, mucocutaneous and visceral forms. The secretion of different cytokines during VL, but another intriguing feature associated with infection is the presence of autoantibodies in the sera of visceral and cutaneous leishmaniasis patients [23] This information has been supported in murine VL, where disease exacerbation is associated with an increased level of IgM, polyclonal B cell activation, and generation of autoantibodies [24]. All this information generates considerable interest in B cells regarding their immune-modulation capacity and involvement in the pathology of VL. We have investigated whether antimony-sensitive and -resistant LD infection modulates splenic B cells and influences secretion of disease-promoting IL-10 from any of the subsets
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