Presented by: Morgan Martin
Vaginal bacterial communities of people across the world are dominated by a few lactobacilli species. Loss of lactobacilli dominance is linked to increased vaginal inflammation with higher levels of pro-inflammatory cytokines. Our work aims to understand how the presence of dominant Lactobacilli species may modulate host immune response to reduce inflammation. We used a human monocyte-derived macrophage reporter cell line, THP1, to screen cell-free supernatants from vaginal lactobacilli for immunomodulatory effects on type I Interferon and NFkB activation and downstream signaling. Addition of cell-free supernatant from vaginal but not intestinal lactobacilli strains suppressed activation of multiple Toll-Like Receptors including TLR2, 3 and 4. Prior activation of cells with TLR agonists induced Interferon and NFkB activation which was suppressed upon addition of cell-free supernatant from vaginal but not intestinal lactobacilli species. Our results suggest that vaginal lactobacilli secrete compounds that suppress inflammatory signaling in human macrophages. With our collaborators, we have screened for and identified active fractions from the supernatant of Lactobacillus crispatus strain MV1A. This work aims to help elucidate the bacterial metabolite(s) responsible for suppression of host TLR signaling pathways. The findings of this study will help increase our understanding of how the lactobacilli-dominated vaginal microbial communities influence host immunity to reduce inflammation.
Morgan Martin – Poster Description (Audio Clip)