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Host intestinal barrier function and immune signaling refers to the integrated physiological system that maintains the separation between the internal host environment and the external luminal contents of the gastrointestinal tract. This system is composed of a physical barrier (epithelial cells and tight junctions), a chemical barrier (mucus and antimicrobial peptides), and an immunological barrier (gut-associated lymphoid tissue and resident immune cells) (Vancamelbeke & Vermeire, 2017; Okumura & Takeda, 2017). Its primary biological function is to facilitate nutrient absorption while preventing the translocation of pathogens and toxins, thereby maintaining systemic homeostasis (Mu et al., 2017). Dysregulation of this system, characterized by increased intestinal permeability and aberrant immune signaling, is a central driver in the pathogenesis of inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis, as well as celiac disease and certain systemic autoimmune conditions (Ghosh et al., 2020). While not a single molecular target, therapeutic interventions often focus on specific components of this system, such as neutralizing pro-inflammatory cytokines (e.g., TNF-alpha, IL-12/23) or blocking lymphocyte trafficking (e.g., alpha-4-beta-7 integrin), to restore barrier integrity and resolve inflammation (Neurath, 2017).
Modulation of the gut-immune axis through cytokine neutralization, inhibition of leukocyte trafficking, or stabilization of epithelial tight junctions.
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