Intestinal epithelial cell–pathogen adhesion interfaces

Intestinal epithelial cell–pathogen adhesion interfaces refer to the specialized molecular contact zones where enteric pathogens, such as Escherichia coli, Salmonella, and Vibrio cholerae, attach to the host's intestinal mucosa to initiate infection [Nature Reviews Microbiology, 2019]. These interfaces are composed of a diverse array of pathogen-encoded adhesins—including pili, fimbriae, and autotransporters—that recognize and bind to specific host receptors such as glycans, integrins, and CEACAM proteins [PubMed, 2021]. While these interactions are fundamental to the pathogenesis of many gastrointestinal diseases, the interface itself is a complex biological structure rather than a single, discrete therapeutic target [Frontiers in Cellular and Infection Microbiology, 2020]. Therapeutic strategies targeting these interfaces, known as anti-adhesion therapies, aim to prevent the initial docking of pathogens, thereby reducing colonization and the subsequent inflammatory response [Journal of Clinical Investigation, 2018]. For example, small molecule inhibitors like Sibofimloc target specific adhesins within these interfaces to treat conditions like Crohn's disease [Enterome, 2022]. However, because this interface involves multiple redundant pathways and varies significantly between different bacterial species, it is classified as a broad biological concept rather than a specific molecular target for drug development [Microbiology and Molecular Biology Reviews, 2016].

Other names

Host-pathogen adhesion interfaceEnteric pathogen-epithelial interfaceMicrobial-mucosal adhesion siteBacterial-epithelial cell interaction

Anti-adhesion agents competitively bind to either the pathogen's adhesins or the host's receptors, physically blocking the formation of the adhesion interface and preventing colonization [Nature Reviews Microbiology, 2017].