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Abstract
Inflammatory bowel disease (IBD) results from alterations in intestinal flora and the immune system. Sulfasalazine (SASP) is a sulfa antimicrobial used to treat IBD in clinic for years. However, how SASP affects gut microbes and its potential functions remains unclear. To investigate the relationships of SASP, IBD, and gut microbiome, we used 2,4,6-trinitrobenzenesulfonic acid (TNBS) to induce experimental colitis in rats, and analyzed the microbiota in the fecal samples, which come from the control group (treated with ethanol + saline), the model group (treated with TNBS-ethanol + saline) and the SASP group (treated with TNBS-ethanol + SASP), with 16S gene sequencing and followed up a subset sample using shotgun sequencing. The study found that SASP treatment could not only restore the TNBS-induced gut dysbiosis, which was proved by the increasing amount of SCFAs-producing bacteria and lactic acid-producing bacteria as well as the decreasing amount of Proteobacteria, but also modulate the dysregulated function of the TNBS-induced colitis to resemble that of the control group, including an increased capacity for basic metabolism (carbohydrate metabolism, citrate cycle) and a decrease in the oxidative stress (riboflavin, sulfur, cysteine) as well as bacterial pathogenesis (cell motility and secretion, bacterial motility proteins, flagellar assembly). Moreover, a higher proportion of Mycoplasma was observed in the SASP group, which may associate with infertility. In all, the study provides insight into specific microbial clades and pathways linked with SASP treatment to elaborate the mechanism for treatment of IBD.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is deemed to arise from a dysregulated immune response to gut microbial communities in individuals with genetic predisposition (Ott et al, 2004; Presley et al, 2012)
After 2 weeks’ trinitrobenzenesulfonic acid (TNBS) administration, rats in the control group and the model group were subjected to gavage with normal saline by equal volume of SASP while the SASP group were orally administered at a dose of 300 mg/kg/day for 16 consecutive days, respectively
The disease activity index (DAI) of the SASP group was significantly lower than that of the model group while it was higher than the control group, implying that colitis with SASP treatment could attenuate inflammation
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is deemed to arise from a dysregulated immune response to gut microbial communities in individuals with genetic predisposition (Ott et al, 2004; Presley et al, 2012). Sulfasalazine Modulates Gut Microbiome many existing therapies are not effective for all patients and some even carry high-risk side effects or complications. High-throughput sequencing can provide us technical support to explore 40% of intestinal flora are uncultured yet (Eckburg et al, 2005), setting a stage for the research of the IBD microbiome. In this case, we intended to explore the effects of SASP on intestinal flora to elaborate the mechanism for treatment of IBD by means of metagenomics
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