M., Hussain, S
Key pathophysiologic mechanisms include: Mucosal barrier dysfunction: Impaired epithelial tight junctions allow bacterial translocation, triggering innate immune activation T-helper cell dysregulation: Predominantly Th1 and Th17 pathways drive chronic inflammation via TNF-, IL-12, IL-23 the basis for biologic therapy targets Transmural inflammation: Unlike UC (mucosal only), CD involves all layers: mucosa submucosa muscularis propria serosa Granuloma formation: Non-caseating granulomas are pathognomonic but present in only ~3050% of biopsies Fibrosis and stricture: Chronic inflammation activates myofibroblasts collagen deposition luminal narrowing obstructive symptoms Fistula formation: Transmural ulcers penetrate serosa form sinus tracts connect to adjacent bowel, bladder, vagina, or skin 7
VSL#3, a multi-strain probiotic mixture, could also be efficacious in inducing remission among individuals with mild to moderate UC [286]
Liegeois et al., 2025)
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Noteworthy, NP seems to be not only promoted by direct injury to neurons but also by TRP channels mediating damage in the surrounding tissue
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