Amal F Al Dawi
Ibn Sina University, Sudan
Title: Modulation of the expression of innate immunity markers by human macrophage THP1 cells following infection with leishmania donovani isolates
Biography
Biography: Amal F Al Dawi
Abstract
Protozoa of the genus Leishmania cause a wide variety of pathologies ranging from self-healing skin lesions to visceral pathology. The outcome of infection depends on the species of the infecting Leishmania parasite. A significant role of the adaptive immune response was described for the development of clinical disease and cure. While TH2 was associated with development of clinical disease, TH1 response was associated with cure. This study aimed to determine the profile of innate immune markers using Leishmania infected human THP1 macrophage cell lines. The parasite isolates were collected from patients suffering from cutaneous, visceral, post kala-azar dermal and mucosal leishmaniasis. Human THP1 cells were infected by live promastiote of Leishmania donovani isolates from Cutaneous (CL), Visceral (VL) and Post Kala-Azar Dermal Leishmaniasis (PKDL) and Mucosal Leishmaniasis (ML) patients. The expression of toll like receptor TL22, TL4 and TL9 and expression of IFN-γ and IL-10 cytokine was measured using Real Time PCR. The production of IL-1ß, IL-6 and TNF-α cytokines was measured using captured ELISA. A significant increase in the expression of TLR 2, TLR4 and TLR9 by L. donovani infected THP-1 from ML patients was detected. A higher concentration IL-6 and IL-1β was detected in supernatants of L. donovani infected human macrophage cell lines from CL patients compared with VL and ML patients whereas IL-1β concentration was higher in L. donovani infected human macrophage cell lines from ML patients. Our data measured a significant increase in the expression of TLR 2 and TNF-α by THP-1 cell line infected with L. donovani isolate from mucosal patient. Leishmania isolates from mucosal and PKDL patients induced significant gene expression of TLR 4 and TLR9. These results could contribute to better understanding of the dynamics of gene expression and production of coinflammatory cytokines in host cells during leishmaniasis.