Recombinant Fasciola hepatica fatty acid binding protein (Fh15) ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice.
Presentation Time: 03:15 PM - 04:30 PM
Poster Board Number: B206
Abstract ID: 4369
Presenting Author:
María Del Mar Figueroa-Gispert , Graduate Student at Univ. de Puerto Rico Recinto de Ciencias Méd.
Abstract:
Ulcerative colitis (UC) is the most common inflammatory bowel disease affecting 5 million individuals worldwide. The Fasciola hepatica-derived molecule termed Fh15 is a TLR4 antagonist that has shown to exhibit powerful anti-inflammatory properties in murine and non-human primate sepsis models. Since TLR4 is involved in UC-pathological mechanisms, we hypothesize that Fh15 will suppress the pathological presentations of UC in mice. To test this hypothesis, we induced UC in C57BL/6 mice by providing animals with 4% DSS drinking water for 7 days. Mice were allotted into three experimental groups and four control groups containing eight mice each (4 male and 4 female). The experimental groups received i.p. injections with 50ug, 100ug or 150ug Fh15 on days 1, 3 and 5 of DSS-drinking. Animals that only drank DSS-water or that only received injections with 50ug, 100ug, or 150ug Fh15 were used as positive and negative controls, respectively. Results demonstrated that Fh15-treated animals had significantly less disease activity index, lower histopathological score, and longer colon-length than DSS-control animals; being 50ug the optimal Fh15 dose to reduce the extension of colon inflammation in male mice. Fh15 also suppressed other inflammatory markers such as MPO, CHI3L1, S100, T cells and macrophages. Preliminary results indicate that Fh15 could be an excellent therapeutic alternative to ameliorate the pathological signs of UC in the mouse model.
Recombinant Fasciola hepatica fatty acid binding protein (Fh15) ameliorates dextran sulfate sodium (DSS)-induced ulcerative colitis in mice.
Category
Poster and Podium (Block Symposium)