In the Journals

Dysbiosis from H. pylori infection may be involved in gastric carcinogenesis

Microbial dysbiosis caused by Helicobacter pylori infection may be an important driver in the development of gastric cancer, according to study results.

Kai-Feng Pan, MD, PhD, of Peking University Cancer Hospital & Institute, and colleagues wrote that previous research has shown that altered microbiota may play a role in gastric carcinogenesis.

“However, whether H. pylori can function as a bacterial driver and interact with other gastric bacteria, which are subsequently involved in the process of carcinogenesis, remains unknown,” they wrote. “Investigation of gastrointestinal microbiota based on a prospective study design following anti-H. pylori treatment may be helpful in exploring the role of H. pylori and its interaction with other bacteria in gastric carcinogenesis.”

Researchers used DNA sequencing to investigate microbial alteration in paired gastric biopsies and stool samples from 58 individuals with successful H. pylori treatment, as well as 57 patients with failed treatment, and compared them with 49 individuals who were H. pylori negative.

Among patients with H. pylori, richness and Shannon indexes increased after eradication and were similar to individuals without H. pylori.

Investigators combined 18 genera that were altered after eradication into a Microbial Dysbiosis Index and found that dysbiotic microbiota in H. pylori positive mucosa was associated with advanced gastric lesions, including chronic atrophic gastritis and intestinal metaplasia/dysplasia. However, this could be reversed by eradication.

Pan and colleagues also found that successful eradication led to increased Bifidobacterium, while failed treatments resulted in more upregulated drug-resistant functional orthologs.

“Successful H. pylori eradication can lead to the restoration of gastric microbiota to a similar status of negative subjects and may exert more beneficial effects on gut microbiota than failed treatment, such as probiotic enrichment and downregulation of drug-resistant mechanism,” they wrote. “Our findings provide new insights into the microbial mechanism of H. pylori-associated gastric carcinogenesis and prevention strategy.” – by Alex Young

Disclosure: The authors report no relevant financial disclosures.

Microbial dysbiosis caused by Helicobacter pylori infection may be an important driver in the development of gastric cancer, according to study results.

Kai-Feng Pan, MD, PhD, of Peking University Cancer Hospital & Institute, and colleagues wrote that previous research has shown that altered microbiota may play a role in gastric carcinogenesis.

“However, whether H. pylori can function as a bacterial driver and interact with other gastric bacteria, which are subsequently involved in the process of carcinogenesis, remains unknown,” they wrote. “Investigation of gastrointestinal microbiota based on a prospective study design following anti-H. pylori treatment may be helpful in exploring the role of H. pylori and its interaction with other bacteria in gastric carcinogenesis.”

Researchers used DNA sequencing to investigate microbial alteration in paired gastric biopsies and stool samples from 58 individuals with successful H. pylori treatment, as well as 57 patients with failed treatment, and compared them with 49 individuals who were H. pylori negative.

Among patients with H. pylori, richness and Shannon indexes increased after eradication and were similar to individuals without H. pylori.

Investigators combined 18 genera that were altered after eradication into a Microbial Dysbiosis Index and found that dysbiotic microbiota in H. pylori positive mucosa was associated with advanced gastric lesions, including chronic atrophic gastritis and intestinal metaplasia/dysplasia. However, this could be reversed by eradication.

Pan and colleagues also found that successful eradication led to increased Bifidobacterium, while failed treatments resulted in more upregulated drug-resistant functional orthologs.

“Successful H. pylori eradication can lead to the restoration of gastric microbiota to a similar status of negative subjects and may exert more beneficial effects on gut microbiota than failed treatment, such as probiotic enrichment and downregulation of drug-resistant mechanism,” they wrote. “Our findings provide new insights into the microbial mechanism of H. pylori-associated gastric carcinogenesis and prevention strategy.” – by Alex Young

Disclosure: The authors report no relevant financial disclosures.

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