Romel Patel
Pronouns: He/Him
Research Mentor(s): Ruma Banerjee
Research Mentor School/College/Department: Biological Chemistry / Medicine
Program:
Authors: Romel Patel, Roshan Kumar, Ruma Banerjee
Session: Session 7: 4:40 pm – 5:30 pm
Poster: 38
Abstract
Microbial metabolism and diet rich in animal protein are sources of hydrogen sulfide (H2S) in host gut and is linked to inflammatory bowel disease (IBD). H2S at lower concentration supports bioenergetics in terms of ATP production but at high concentrations blocks the complex IV of mitochondria and act as a respiratory toxin. Our understanding of how chronic exposure to microbial or diet derived H2S affects host metabolism is limited. Preliminary data generated in the lab showed methionine, which is abundant in animal proteins increases thiosulfate, a marker of H2S homeostasis, decreases colonic goblet cell density and changes microbial populations . Goblet cells secrete mucus and forms a chemical barrier between host and its microbiota. Steady-state H2S levels in host cells are regulated by its rates of production and disposal via a mitochondrial oxidation pathway. Sulfide quinone oxidoreductase (SQOR) catalyzes the first step in the oxidation pathway, using CoQ as an electron acceptor, which couples H2S oxidation to the electron transport chain (ETC) at the level of complex III. Higher levels of sulfide either due to increased production or lowered clearance impact host cell function and induces a reductive metabolic shift. It is important to understand the contribution of sulfide production through host as well as microbiota. I have standardized a semi-quantitative sulfide detection assay produced by fecal microbiota through cysteine desulfurase activity. When sulfide contacts the lead acetate it produces lead sulfide which forms black participate on paper. Using this strategy I have identified that germ-free mice have lowered sulfide producing capacity compared to conventional mice. The significance of this study is that it will allow assessment of how the three-way interaction between diet-genotype-gut microbiome affects H2S metabolism and modulates IBD.
