Sly Saint
Senior Member (Voting Rights)
Although it is one of the oldest medications used to treat patients with inflammatory bowel disease (IBD) and an effective treatment for an associated arthritis condition called spondyloarthritis (SpA), sulfasalazine's mechanism of action has been unclear. Now researchers at the Jill Roberts Center for IBD and the Jill Roberts Institute for Research in IBD at Weill Cornell Medicine and NewYork-Presbyterian have determined that the drug works by modulating the activity of a group of gut bacteria that are more abundant in patients who respond to the drug. These findings solve a long-standing question of how and why sulfasalazine is effective for some people, but not all, and could lead to advances in treating IBD.
In a study published Feb. 19 in Cell Reports Medicine, researchers examined IBD-SpA patients treated with sulfasalazine and found that the presence of the gut bacterium Faecalibacterium prausnitzii was a key factor enabling successful treatment responses. They determined that sulfasalazine works by upregulating this bacterium's production of butyrate, a fatty acid molecule with anti-inflammatory properties.
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IBD frequently coexists with SpA, and sulfasalazine reduces or eliminates symptoms of both conditions in many of these patients. Prior studies have suggested that it works via the gut microbiome, though the precise mechanism has never been clear.
Unlocking sulfasalazine's mechanism of action in IBD-SpA patients (msn.com)