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08

2024

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09

Yu Jun/Shen Zuyao of the Chinese University of Hong Kong found that in addition to Helicobacter pylori, infection with Streptococcus angina can also cause gastritis/gastric cancer

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Gastric mucosa in patients with gastric cancer (GC) is rich in angina streptococci (S. anginosus）。

Recently, the Chinese University of Hong Kong and Shen Zuyao (Joseph Jao-Yiu SUNG) jointly communicated inCell Online published the title"Streptococcus anginosuspromote gastric inflammation， atrophy， and tumorigenesis in miceThe study found thatStreptococcus angustifolia colonizes and induces acute gastritis in the stomach of mice.Streptococcus pharyngitis infection spontaneously induced progressive chronic gastritis, parietal cell atrophy, mucous metaplasia, and dysplasia in regular mice, a finding also confirmed in germ-free mice. Furthermore, in carcinomatous-induced gastric tumorigenesis and YTN16 GC cell allograft, Streptococcus anginosus accelerated the progression of GC. Consistent with this, Streptococcus angina disrupts gastric barrier function, promotes cell proliferation, and inhibits apoptosis.

Mechanically, the study found a surface protein TMPC of Streptococcus angina that interacts with the annexin A2 (ANXA2) receptor on gastric epithelial cells. Interaction of TMPC with ANXA2-mediated attachment and colonization of Streptococcus angina and induction of mitogen-activated protein kinase (MAPK) activation. Knockout of ANXA2 abolished induction of MAPK by Streptococcus angina.Thus, the present study revealed that S. pharyngitis is a pathogen that promotes gastric tumorigenesis through direct interaction with gastric epithelial cells on the TMPC-ANXA2-MAPK axis.

 

Gastric cancer (GC) is the fifth most common cancer worldwide and the leading cause of cancer death. Helicobacter pylori (Helicobacter pylori, H. pylori) is a major risk factor for gastric cancer and has been classified as a type I carcinogen.H. pylori infection promotes gastritis, atrophy and intestinal metaplasia (IM). In H. pylori-infected individuals, only 1%-3% eventually develop GC, inferring the involvement of other factors. Emerging evidence suggests that there is a large non-Helicobacter pylori microbiota in the gastric mucosa and that their dysregulation may play a role in gastric carcinogenesis. However, the identification and characterization of non-Helicobacter pylori drivers associated with gastric carcinogenesis remains unexplored.

In order to explore the gastric microbiota of non-Helicobacter pylori, researchers characterized the gastric microbiota of Helicobacter pylori-negative patients. Five GC-rich oral pathogens, including Streptococcus angina (S. anginosus）。Angitis streptococcus is a gram-positive, non-spore-forming, inactive bacteria, mainly in the mouth, nasopharynx, gastrointestinal tract and vagina, can cause abscess and other invasive suppurative infections. Angiomycosis streptococci have a marked adaptability to low pH conditions (pH 3-5), which may contribute to their survival in the gastric mucosa.however,angina streptococcusThe role in the development of gastric cancer and its pathogenic molecular mechanisms are largely unknown.

In this study, Streptococcus angina was identified as a non-Helicobacter pylori pathogen that can rapidly cause acute gastritis after long-term infection of regular and germ-free mice, resulting in chronic gastritis, gastric mucus metaplasia, and dysplasia.Angina streptococcus accelerates the occurrence of gastric cancer. In terms of mechanism, the study found that the surface protein TMPC of Streptococcus angina directly interacts with the gastric epithelial cell receptor annexin A2 (ANXA2) to colonize the gastric mucosa and mediate the activation of mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, the study defines a non-Helicobacter pylori pathogen, that is, a direct cause of gastric tumor angina streptococcus .

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