The mechanism that links a common ingredient in toothpaste to inflammatory bowel disease has been revealed, raising questions about the wisdom of its use in several health products.
Clean teeth are an expected aspect of modern life, one that most of us would expend a great deal of effort and expense to maintain. But could some elements of our current oral hygiene regimen be leading to issues elsewhere? Recently, the antimicrobial triclosan – an ingredient in many toothpastes – has been indicated as a stimulant of colitis in mice. But this is not the first time that this chemical has been highlighted as a threat.
In 2016 the use of triclosan in soap was banned by the FDA due to its supposed contributions to the rise of antibiotic resistant bacteria. However, evidence pertaining to its impact on the gut is yet to see it removed from toothpastes, where it has been shown to prevent gingivitis, a mild form of gum disease, and from bacteria-resistant athletic clothing.
A recent multicentre collaboration between the several universities in the USA and Hong Kong, led by the University of North Carolina at Chapel Hill (NC, USA), has identified the bacteria and enzymes involved in the mediation of triclosan’s harmful effects on the gut. The study provides key details to support the mounting evidence that triclosan aggravates the intestines, leading to conditions such as colitis and irritable bowel disease.
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Triclosan is known to be rapidly metabolized in tissues such as the liver, to form the conjugate TCS-glucuronide (TCS-G), which is harmless and is rapidly eliminated from the body. Previous studies have demonstrated that triclosan promotes colonic inflammation in mice but is unable to do so in germ free mice with no gut microbiome. This indicates that the gut microbiome plays a role in the reactivation of TCS-G to free triclosan.
To investigate the mechanism in the gut that activates triclosan, the team deployed LC-MS/MS in a series of experiments in both mouse and human models to analyze the metabolic profiles of triclosan in different sections of the gut and under different administration regimens. Following this a series of in vitro gut microbial culture and in vivo microbial suppression experiments were used to determine the bacteria responsible for the conversion TCS-G into the free and active triclosan.
The team first found that the bacterial β-glucuronidase (GUS) enzymes played a key role in activating triclosan. Targeted inhibition of the GUS enzymes in mice prevented the colitis promoting effects of tricolsan in mice.
The team sees this as a major breakthrough in the fight against the rising tide of inflammatory bowel disease diagnoses, both in preventing the aggravation of the condition – so called ‘flare ups’ – and in developing potential treatments for it.
What’s more, after observing the ready uptake of triclosan into the gut of human study participants provided with triclosan containing products such as toothpaste, the authors are keen for regulatory bodies to reconsider the use of the antimicrobial all together. The paper concludes that, “the safety of TCS and related compounds should be reconsidered given their potential for intestinal damage.”