Helicobacter pylori - CEACAM interaction, gastric leukocyte recruitment and local immunomodulation (B05)

幽门螺杆菌可能导致消化性溃疡或胃癌。这种细菌使用CEACAM宿主细胞受体注入其CagA毒素。幽门螺杆菌不与小鼠CEACAMs相互作用，从而阻止细胞信号转导和随后小鼠白细胞中趋化因子的释放，防止免疫细胞在胃粘膜中的强烈募集。我们的目标是对表达人CEACAMs的小鼠白细胞进行功能鉴定，并利用生物化学和新颖的多光子活体显微镜研究它们与幽门螺杆菌在体外和体内的相互作用，以更好地了解幽门螺杆菌在宿主中的持续机制。

Helicobacter pylori may cause peptic ulcer or gastric cancer. The bacteria use CEACAM host cell receptors to inject its CagA toxin. H. pylori does not interact with murine CEACAMs, which prevents cellular signaling and subsequent chemokine release in murine leukocytes, preventing a strong recruitment of immune cells in the gastric mucosa. We aim to functionally characterize murine leukocytes expressing human CEACAMs and investigate their interaction with H. pylori in vitro and in vivo using biochemical and novel multiphoton intravital microscopy to better understand the persistence mechanisms of H. pylori in the host.