Wednesday, 4 October 2017

Perturbing Transsulfuration Pathway and Sulfur Recycling, A New Direction Towards Therapeutic Intervention of Inflammatory Bowel Disease

Combating inflammatory bowel disease (IBD) is becoming a growing challenge to the global health management. Our bowel can be envisioned as a big vessel reactor where millions of reactions occur at each moment, every day to meet the physiological demand of our body for quality control of our life. This includes the orchestration of several steps which ultimately funnel down to the intestinal system to drives the end point of the digestion process. Intestinal sulfur recycling by transsulfuration pathway can modulates the integrity of our bowel symptoms. Limiting the sulfur amino acid metabolism and mitigating hydrogen sulfide (H2S) generation can help to stabilize the colonic biochemistry with monitoring of metabolites for subsequent health risk assessment. Regulating protein sulfhydration in colonic tissue could play detrimental roles in the modulation of several contributing factors related to IBD.

Our bowel is challenged daily with a load of foods, primarily sourced from the environment. Many food components contain sulfides, polysulfide compounds, which ultimately breakdown to generate gaseous H2 S in situ. Hydrogen sulfide can interact with metabolic cytochrome c oxidase and carbonic anhydrase, by chelating with metalbinding porphyrin cofactor. Evolutionarily, H2 S has been viewed as an important prebiotic element. In nature, H2 S concentration increases in the deep ocean, oceanic volcanoes and mountain spring while the oxygen concentration decreases. Importantly, hydrogen sulfide can bypass the cellular oxygen demand and modulate energy production.

There are many micro bacteria that can produce H2 S. Some of these bacteria exist in the gut mucosal system of our gastrointestinal tract [8, 9]. Examples of these bacteria include sulfate reducing bacteria (SRB), thiobacillus, desulfobacter among others. Some of this microbiota could play a potent role during GI infection and inflammation, and thus could be one of the leading causes of IBD. Therefore, H2 S producing colonic microbiota in the GI tract can also modulate the mucosal immune system, and the IBD state, by producing H2 S or sulfur metabolites.

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