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Triclosan and triclocarban as potential risk factors of colitis and colon cancer: Roles of gut microbiota involved

Journal

SCIENCE OF THE TOTAL ENVIRONMENT
Volume 842, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.scitotenv.2022.156776

Keywords

Triclosan (TCS); Triclocarban (TCC); In flammatory bowel disease (IBD); Colon cancer; Gut microbiota; Gut microbial metabolism

Funding

  1. University of Massachusetts Amherst
  2. USDA NIFA [2019-67017-29248, 2020-67017-30844]
  3. USDA/Hatch [MAS00556]

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In recent years, there has been a significant increase in the occurrence of inflammatory bowel disease (IBD), a chronic inflammatory disease of the intestines. Exposure to the chemicals triclosan (TCS) and triclocarban (TCC) may contribute to the development of IBD and associated diseases, as studies have shown that exposure to these chemicals increases the severity of colitis and exacerbates colon tumorigenesis in mice. The presence of gut microbiota is necessary for the toxic effects of these compounds.
In recent decades there has been a dramatic increase in the incidence and prevalence of inflammatory bowel disease (IBD), a chronic inflammatory disease of the intestinal tissues and a major risk factor of developing colon cancer. While accumulating evidence supports that the rapid increase of IBD is mainly caused by exposure to environmental risk factors, the identities of the risk factors, as well as the mechanisms connecting environmental exposure with IBD, remain largely unknown. Triclosan (TCS) and triclocarban (TCC) are high-volume chemicals that are used as antimicrobial ingredients in consumer and industrial products. They are ubiquitous contaminants in the environment and are frequently detected in human populations. Recent studies showed that exposure to TCS/TCC, at human exposure relevant doses, increases the severity of colitis and exacerbates colon tumorigenesis in mice, suggesting that they could be risk factors of IBD and associated diseases. The gut toxicities of these compounds require the presence of gut microbiota, since they fail to induce colonic inflammation in mice lacking the microbiota. Regarding the functional roles of the microbiota involved, gut commensal microbes and specific microbial beta-glucuronidase (GUS) enzymes mediate colonic metabolism of TCS, leading to metabolic reactivation of TCS in the colon and contributing to its subsequent gut toxicity. Overall, these results support that these commonly used compounds could be environmental risk factors of IBD and associated diseases through gut microbiota-dependent mechanisms.

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