Galectin-8, a beta-galactoside-binding lectin, is upregulated in the gastric tissues of rhesus macaques infected with Helicobacter pylori. In this study, we found that H. pylori infection triggers intracellular galectin-8 aggregation in human-derived AGS gastric epithelial cells, and that these aggregates colocalize with lysosomes. Notably, this aggregation is markedly reduced following the attenuation of host O-glycan processing. This indicates that H. pylori infection induces lysosomal damage, which in turn results in the accumulation of cytosolic galectin-8 around damaged lysosomes through the recognition of exposed vacuolar host O-glycans. H. pylori-induced galectin-8 aggregates also colocalize with autophagosomes, and galectin-8 ablation reduces the activation of autophagy by H. pylori. This suggests that galectin-8 aggregates may enhance autophagy activity in infected cells. We also observed that both autophagy and NDP52, an autophagy adapter, contribute to the augmentation of galectin-8 aggregation by H. pylori. Additionally, vacuolating cytotoxin A, a secreted H. pylori cytotoxin, may contribute to the increased galectin-8 aggregation and elevated autophagy response in infected cells. Collectively, these results suggest that H. pylori promotes intracellular galectin-8 aggregation, and that galectin-8 aggregation and autophagy may reciprocally regulate each other during infection.

中文翻译：

---

幽门螺杆菌以宿主O-聚糖依赖性方式诱导胃上皮细胞内受损溶酶体周围的细胞内galectin-8聚集

Galectin-8（一种β-半乳糖苷结合凝集素）在感染了幽门螺杆菌的恒河猴的胃组织中被上调。在这项研究中，我们发现幽门螺杆菌感染会触发人源性AGS胃上皮细胞中的细胞内半乳糖凝集素8聚集，并且这些聚集体与溶酶体共定位。值得注意的是，随着宿主O-聚糖加工的减弱，这种聚集显着减少。这表明幽门螺杆菌感染会引起溶酶体损伤，进而通过识别暴露的液泡宿主O-聚糖，导致受损溶酶体周围胞质半乳糖凝集素8的积累。幽门螺杆菌诱导的galectin-8聚集体也与自噬体共定位，而galectin-8消融可减少幽门螺杆菌对自噬的激活。这表明galectin-8聚集体可以增强感染细胞中的自噬活性。我们还观察到自噬和自噬适配器NDP52都有助于幽门螺杆菌对galectin-8聚集的增强。此外，空泡细胞毒素A，一种分泌的幽门螺杆菌细胞毒素，可能有助于受感染细胞中半乳糖凝集素8聚集的增加和自噬反应的升高。总的来说，这些结果表明幽门螺杆菌 促进细胞内半乳糖凝集素8的聚集，而半乳糖凝集素8的聚集和自噬在感染过程中可能相互调节。