Abstract
Helicobacter pylori is recognised as a main risk factor for gastric cancer. However, approximately half of the patients with gastritis are negative for H. pylori infection, and the abundance of H. pylori decreases in patients with cancer. In the current study, we profiled gastric epithelium-associated bacterial species in patients with gastritis, intestinal metaplasia, and gastric cancer to identify additional potential pathogenic bacteria. The overall composition of the microbiota was similar between the patients with gastritis and those with intestinal metaplasia. H. pylori was present in half of the non-cancer group, and the dominant bacterial species in the H. pylori-negative patients were Burkholderia, Enterobacter, and Leclercia. The abundance of those bacteria was similar between the cancer and non-cancer groups, whereas the frequency and abundance of H. pylori were significantly lower in the cancer group. Instead, Clostridium, Fusobacterium, and Lactobacillus species were frequently abundant in patients with gastric cancer, demonstrating a gastric cancer-specific bacterial signature. A receiver operating characteristic curve analysis showed that Clostridium colicanis and Fusobacterium nucleatum exhibited a diagnostic ability for gastric cancer. Our findings indicate that the gastric microenvironment is frequently colonised by Clostridium and Fusobacterium in patients with gastric cancer.
Highlights
The extreme acidity and thick protective mucosa of the gastric environment limit the growth and colonisation of bacteria
H. pylori infection has been identified as the strongest risk factor for gastric cancer, only approximately half of all patients with gastritis are infected with H. pylori[18,19]
According to their pathological reports, the patients enrolled were assigned to the gastritis, intestinal metaplasia, or cancer groups
Summary
The extreme acidity and thick protective mucosa of the gastric environment limit the growth and colonisation of bacteria. Secretory machinery that is encoded by the cag pathogenicity island[14] This system is used to deliver the virulence factors CagA and peptidoglycan to the gastric mucosal cells[15,16]. Peptidoglycan activates the PI3K-Akt signalling pathway to decrease apoptosis and promote cell migration[13,17] Together, these virulence factors produced by H. pylori facilitate the transformation of gastric mucosal cells and lead to a drastic increase in the risk of gastric cancer. A hypothesis to account for the decline in the abundance of H. pylori in gastric cancer is microbial succession[10] This hypothesis proposes that H. pylori creates a niche microenvironment on the gastric mucosa that facilitates its colonisation by secondary settler bacteria. The enrichment of Fusobacterium and Clostridium raises the possibility that those bacteria may be involved in gastric oncogenesis
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