Suppression of Helicobacter pylori Infection With Bismuth Subsalicylate: Was It the Bismuth or the Salicylate?

To the EDITOR—I read with great interest the publication by Geng et al [1] on their serendipitous observation that bismuth subsalicylate suppressed gastric infection in a patient with drug-resistant Helicobacter pylori. The purpose of this communication is to consider which of the components of the combination, or both, might be responsible for the efficacy of bismuth subsalicylate. The authors have reviewed the potential effects of bismuth. This letter focuses on the ability of the salicylate component to suppress flagella. There is convincing evidence that the motility of H pylori flagella has a key role in the colonization of the human gastric mucosa [2]. Mice immunized with a vaccine targeting H pylori flagella significantly reduced colonization [3]. The immune system has an extensive array of protective mechanisms to corral colonic flagellated microbiota [4]. These include the Toll-like receptor 5 that senses flagellin and the NOD-like receptor 4. On detection of flagellin, this receptor protein activates the inflammasome. Salicylate reversibly blocks the synthesis of flagellin and flagella in enteric gram-negative bacteria and may protect against an inflammatory response [5]. This supports the notion that the salicylate component of bismuth subsalicylate is an active ingredient against H pylori. This hypothesis is offered to stimulate further work in this important field.

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Potential conflicts of interest. The author: No reported conflicts.

The author has submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.