Immune response and inflammatory pathway of ulcerative colitis

Abstract

Ulcerative colitis (UC) is an idiopathic relapsing inflammatory disease. Although the etiology of UC remains unclear, it could be characterized by inflammation of the intestinal mucosa, starting from the rectum and potentially involving the entire colon. The immune response and inflammatory pathway of UC have shown that tissue damage is driven by dynamic and complexes of cells and cytokines. Various types of cells, including antigen-presenting cells (dendritic cells and macrophages), T helper cells, regulatory T cells, and natural killer T cells, play a crucial role in UC pathogenesis by regulation, suppression, and maintenance of inflammation. Moreover, cytokine networks become an important part due to their signaling function, which is indispensable for cell communication. Pro-inflammatory cytokines [tumor necrosis factor-α, interleukin (IL)-1, IL-6, IL-9, IL-13, and IL-33] play significant roles in upregulation, while anti-inflammatory cytokines (transforming growth factor-β, IL-10, and IL-37) play significant roles in downregulation of disease progression. The pathogenesis of UC consists of immuno-inflammatory pathways related to the multiple components of the intestine, including the epithelial barrier, commensal microflora, antigen recognition, dysregulation of immunological responses, leukocyte recruitment, and genetic factors. The understanding of immuno-inflammatory pathways of UC might lead to the development of a specific therapy and/or a novel treatment that could be more efficient.

Lactobacillus plantarum L15 Alleviates Colitis by Inhibiting LPS-Mediated NF-κB Activation and Ameliorates DSS-Induced Gut Microbiota Dysbiosis

“…One type of cytokine, the TNF-α has been linked with pro-inflammatory responses. Similarly, another category of cytokines secreted from macrophages, the IL-1β, is involved in pro-inflammatory regulations that facilitates UC progression ( 48 ). In addition, T and natural killer cells are mediated by the IL-12 cytokine, which in turn fuels TNF-α secretion ( 49 ).…”

Exosomes from mesenchymal stromal cells reduce murine colonic inflammation via a macrophage-dependent mechanism

“…Dysregulation of inflammatory mediators and disruption of intestinal barrier integrity in IBD patients and in experimental colitis often interact in a positive feedback loop, together forming a vicious cycle (29)(30)(31). MSC-Exos treatment could serve dual roles to break this cycle, by reducing a panel of inflammatory mediators and maintaining intestinal homeostasis.…”

Gut microbiota in ulcerative colitis: insights on pathogenesis and treatment

“…The homeostasis of T cells (regulatory and effector cells, Th1, Th2 and Th17) is disturbed in patients with UC, resulting in inflammation. Furthermore, UC pathogenesis is considered an atypical Th2 response mediated by a distinct subset of natural killer T cells that produce interleukin‐13 and damage epithelial cells . The loci‐specific risk for UC plays an important role in the immune reaction mediating UC pathogenesis.…”

“…The loci‐specific risk for UC plays an important role in the immune reaction mediating UC pathogenesis. Thus, an improved understanding of UC pathogenesis, including immune response and inflammatory pathways, may lead to the development of a more efficient therapy for UC …”