Pathophysiology updates: gastroduodenal injury and repair mechanisms

Although the mucosal barrier serves as a primary interface between the environment and host, little is known about the repair of acute, superficial lesions or deeper, persistent lesions that if not healed, can be the site of increased permeability to luminal antigens, inflammation, and/or neoplasia development.

Recent studies on acute superficial lesions have focused on calcium signaling and focal adhesion kinase, which regulate cell migration and controlled matrix adhesion during restitution. Microfluidic organ-on-a-chip and gut-on-a-chip models continued in development to support reductionist studies of epithelial-bacterial and/or epithelial-immune cell interactions during mucosal barrier disruption. In fact, these models may allow personalized medicine studies in the future using patient-derived cells to evaluate injury and repair mechanisms. Work done in the past year evaluated the safety and efficacy of acid blocking drugs on ulcer healing, with new animal studies providing evidence that each drug affects the microbiome in a different way that can be correlated with its efficacy in ulcer healing. Lastly, work to understand the way in which mature epithelial cells or committed stem cells dedifferentiate, reprogram, proliferate, and then regenerate the gastroduodenal mucosa after injury was a major focus of studies in the past year.

Recent studies highlight novel mechanisms that promote restitution and mucosal regeneration after injury of the gastroduodenal mucosa.