Differential RNA expression of peritoneal macrophages infected with antimony-sensitive (LD-S) antimony-unresponsive (LD-R) at 4hrs, 24hrs, and 48hrs post-infection keeping uninfected macrophages as control.

Recent clinical LD field isolates still showed antimony resistance (LD-R) even after the withdrawal of pentavalent antimonials in treating Visceral leishmaniasis in India decades back due to the emergence of antimony resistance. Clinical infection with LD-R results in aggressive pathogenesis characterized by higher parasite burden, chronic hepatosplenomegaly, and severe anemia, the reason of which is poorly understood. Thus, it is paramount to unveil the underlying signaling contributing to severe anemia and chronic hepatosplenomegaly resulting from parasite overburden observed in LD-R infection. Our data provides insights into how LD-R modulates murine macrophages in-vitro to proliferate rapidly while dodging off the host immune surveillance at the host-parasite interface at early and late time points of infection as compared to its sensitive counterparts. Overall design: Murine peritoneal macrophages were infected with AG83 (LD-S) and BHU575 (LD-R) at 4hrs, 24hrs, and 48hrs keeping uninfected macrophages as control. Each experimental sets are kept in duplicates. Total RNA was isolated from the experimental samples. The main objective of RNAseq analysis was to check the differential gene expression of LD-S vs LD-R infected macrophages at early and late time points at the host-parasite interface to unveil the differential host modulation by the semsitive and unresponsive LD isolates.