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Gut check: can other microbes or communities phenocopy H. pylori’s early gastric pathology?
  1. Jeffrey W Brown
  1. Department of Medicine, Washington University in St Louis School of Medicine, St Louis, MO 63110-1010, USA
  1. Correspondence to Dr Jeffrey W Brown, Department of Medicine, Division of Gastroenterology, Washington University in St Louis School of Medicine, St Louis, MO 63110-1010, USA; brownjw{at}

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The gastric mucosa is exposed to billions of diverse microorganisms every day. To stymie gastric colonisation as well as to limit passage of potential pathogens to more distal segments of the GI tract, the stomach has several broadly active defence mechanisms: acidity, mucus and proteolytic enzymes. Other extragastric mechanisms may contribute: for example, glycosylation epitopes like 3′-Sulfo-Lewis A on salivary mucins cotransit with swallowed bacteria and associate with them when the pH drops in the stomach,1 presumably preventing the bacteria from binding the mucosa.

Despite these defenses, at least one bacterial species, Helicobacter pylori is able to colonise the human stomach. This pathogen initially invades the gastric antrum, but it can also spread to the gastric body by inducing a metaplastic glandular response,2 characterised by loss of acid-secreting parietal cells (oxyntic atrophy) and metaplastic glandular changes (ie, Spasmolytic Expressing Polypeptide Metaplasia or SPEM). In a small proportion of individuals, metaplasia can progress to dysplasia and gastric adenocarcinoma. Thus, identifying the early histological changes associated with H. pylori infection becomes clinically important.3

The decrease in or absence of acidity associated with oxyntic atrophy creates an environment permissive for colonisation by opportunistic microbes. Although the presence of these ectopic microbial communities correlates with oxyntic atrophy,4 previously there has been no clear demonstration that …

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  • Twitter @JeffreyWadeBro1

  • Contributors I conceived of and wrote the manuscript.

  • Funding JWB is supported by the Department of Defence, through the PRCRP programme under Award No. W81XWH-20-1-0630, P30 DK052574, the American Gastroenterological Association AGA2021-5101, R21 AI156236, and the Doris Duke Fund to Retain Clinical Scientists.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting or dissemination plans of this research.

  • Provenance and peer review Commissioned; internally peer reviewed.

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