Abstract
The development of sequencing technology has expanded our knowledge of the human gastric microbiome, which is now known to play a critical role in the maintenance of homeostasis, while alterations in microbial community composition can promote the development of gastric diseases. Recently, carcinogenic effects of gastric microbiome have received increased attention. Gastric cancer (GC) is one of the most common malignancies worldwide with a high mortality rate. Helicobacter pylori is a well-recognized risk factor for GC. More than half of the global population is infected with H. pylori, which can modulate the acidity of the stomach to alter the gastric microbiome profile, leading to H. pylori-associated diseases. Moreover, there is increasing evidence that bacteria other than H. pylori and their metabolites also contribute to gastric carcinogenesis. Therefore, clarifying the contribution of the gastric microbiome to the development and progression of GC can lead to improvements in prevention, diagnosis, and treatment. In this review, we discuss the current state of knowledge regarding changes in the microbial composition of the stomach caused by H. pylori infection, the carcinogenic effects of H. pylori and non-H. pylori bacteria in GC, as well as the potential therapeutic role of gastric microbiome in H. pylori infection and GC.
Highlights
Gastric cancer (GC) is the third leading cause of cancer death after lung and colorectum cancers, and accounts for 782,685 deaths worldwide each year (Bray et al, 2018)
To gain a better understanding of the relationship between the gastric microbiome and gastric carcinogenesis, here we provide an update on the gastric microbiome in healthy state and H. pylori-associated pathological conditions, including gastritis, peptic ulcer disease, and GC
Only a small proportion of patients with H. pylori infection or who use non-steroidal anti-inflammatory drugs (NSAIDs) progress to peptic ulcer disease, suggesting that decreased mucosal resistance to bacterial virulence factors and drug toxicity contribute to its pathogenesis (Lanas and Chan, 2017)
Summary
Gastric cancer (GC) is the third leading cause of cancer death after lung and colorectum cancers, and accounts for 782,685 deaths worldwide each year (Bray et al, 2018). An examination of patients at different histologic stages of gastric carcinogenesis (gastritis, gastric intestinal metaplasia, and GC) revealed an inverse relationship between H. pylori abundance and microbial diversity in non-cancer gastric biopsies, but GC was associated with a lower diversity compared to other samples with similar H. pylori abundance; the difference was abrogated by antibiotic treatment (Li et al, 2017). Only a small proportion of patients with H. pylori infection or who use NSAIDs progress to peptic ulcer disease, suggesting that decreased mucosal resistance to bacterial virulence factors and drug toxicity contribute to its pathogenesis (Lanas and Chan, 2017). Another study in Malaysian patients showed similar microbiome profiles in H. pylori-positive and -negative patients as well as an association between the isolation of Streptococci and peptic ulcer disease, suggesting that Streptococci colonize the stomach and that their interactions with H. pylori contribute to the development of peptic ulcer disease (Khosravi et al, 2014). 21 superficial gastritis, 23 atrophic gastritis, 17 intestinal metaplasia and 20 gastric cancer subjects
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