The intestinal epithelium limits host-luminal interactions and maintains gut homeostasis. Breakdown of the epithelial barrier and villous atrophy are hallmarks of coeliac disease. Besides the well characterized immune-mediated epithelial damage induced in coeliac mucosa, constitutional changes and early gluten direct effects disturb intestinal epithelial cells. The subsequent modifications in key epithelial signaling pathways leads to outnumbered immature epithelial cells that, in turn, facilitate epithelial dysfunction, promote crypt hyperplasia, and increase intestinal permeability. Consequently, underlying immune cells have a greater access to gluten, which boosts the proinflammatory immune response against gluten and positively feedback the epithelial damage loop. Gluten-free diet is an indispensable treatment for coeliac disease patients, but additional therapies are under development, including those that reinforce intestinal epithelial healing. In this chapter, we provide an overview of intestinal epithelial cell disturbances that develop during gluten intake in coeliac disease mucosa.

肠上皮细胞限制宿主-管腔相互作用并维持肠道稳态。上皮屏障的破坏和绒毛萎缩是乳糜泻的标志。除了在腹腔黏膜中诱导的明确表征的免疫介导的上皮损伤外，体质变化和早期麸质直接作用会干扰肠上皮细胞。随后对关键上皮信号通路的修改导致数量超过未成熟上皮细胞，进而促进上皮功能障碍、促进隐窝增生和增加肠道通透性。因此，潜在的免疫细胞更容易获得麸质，从而增强针对麸质的促炎免疫反应，并积极反馈上皮损伤循环。无麸质饮食是乳糜泻患者不可缺少的治疗方法，但其他疗法正在开发中，包括那些加强肠上皮愈合的疗法。在本章中，我们概述了在乳糜泻黏膜摄入麸质期间出现的肠上皮细胞紊乱。