大量研究表明，浅表性胃炎（SG）和萎缩性胃炎（AG）是胃癌（GC）的先兆。虽然幽门螺杆菌 (H. pylori) 长期以来一直被认为是 GC 发展的关键参与者，但 Fu 等人的最新发现。已确定咽峡炎链球菌 (S.anginosus) 是一种新出现的病原体，可引发 SG、AG 和 GC。咽峡炎链球菌是一种革兰氏阳性球菌，利用其表面蛋白梅毒螺旋体膜蛋白 C (TMPC) 与胃上皮细胞的膜联蛋白 A2 (ANXA2) 受体结合，促进其在胃粘膜中的定植和侵袭。这导致促炎趋化因子 Ccl20 和 Ccl8 上调，对胃屏障功能和微生物群稳态造成长期影响，从而导致 SG。此外，这些细菌还激活丝裂原激活蛋白激酶 (MAPK) 信号通路，该通路与 AG 和 GC 的发育相关。重要的是，抑制 TMPC 或敲低 ANXA2 可以减少咽峡炎链球菌定植和侵袭，从而降低 SG、AG 和 GC 的机会。本文重点介绍了咽峡炎链球菌在 SG、AG 和 GC 中的分子机制，强调多病原体策略在胃病管理中的重要性以及进一步研究咽峡炎链球菌在 GC 进展中的作用的必要性。

A wealth of research indicates that superficial gastritis (SG) and atrophic gastritis (AG) are precursors to gastric cancer (GC). While Helicobacter pylori (H. pylori) has long been recognized as a key player in GC development, recent findings by Fu et al. have identified Streptococcus anginosus (S. anginosus) as an emerging pathogen that can trigger SG, AG and GC. S. anginosus, a gram-positive coccus, leverages its surface protein T. pallidum membrane protein C (TMPC) to engage with the annexin A2 (ANXA2) receptor of gastric epithelial cells, facilitating its colonization and invasion in the gastric mucosa. This leads to an upregulation of proinflammatory chemokines Ccl20 and Ccl8, causing prolonged effects on gastric barrier function and microbiota homeostasis, leading to SG. Moreover, these bacteria activate the mitogen-activated protein kinase (MAPK) signaling pathway, which is associated with the development of AG and GC. Importantly, inhibiting TMPC or knocking down ANXA2 can reduce S. anginosus colonization and invasion, lowering the chances of SG, AG, and GC. This paper highlights the molecular mechanisms of S. anginosus in SG, AG and GC, emphasizing the importance of a multi-pathogen strategy in gastric disease management and the need for further investigation into the role of S. anginosus in GC progression.