Beteiligung biologischer Wege an der Entwicklung entzündlicher Darmerkrankungen

Abstract

Apoptosis, autophagy and necrosis are three distinct functional types of the mammalian cell death network. All of them are characterized by a number of cell's morphological changes. The inappropriate induction of cell death is involved in the pathogenesis of a number of diseases.Pathogenesis of inflammatory bowel diseases (ulcerative colitis, Crohn's disease) includes an abnormal immunological response to disturbed intestinal microflora. One of the most important reason in pathogenesis of chronic inflammatory disease and subsequent multiple organ pathology is a barrier function of the gut, regulating cellular viability. Recent findings have begun to explain the mechanisms by which intestinal epithelial cells are able to survive in such an environment and how loss of normal regulatory processes may lead to inflammatory bowel disease (IBD).This review focuses on the regulation of biological pathways in development and homeostasis in IBD. Better understanding of the physiological functions of biological pathways and their influence on inflammation, immunity, and barrier function will simplify our expertice of homeostasis in the gastrointestinal tract and in upgrading diagnosis and treatment.

Identification of Candidate Genes Related to Inflammatory Bowel Disease Using Minimum Redundancy Maximum Relevance, Incremental Feature Selection, and the Shortest-Path Approach

“…SLTM (rank 4 in the mRMR feature list) acts as a general inhibitor of transcription that eventually leads to apoptosis via the regulation of telomere [ 73 ]. Because IBD is associated with abnormal cell death, SLTM may participate in IBD through the regulation of the apoptosis of intestinal cells [ 74 ]. CNOT8 (rank 14 in the mRMR feature list) is a significant predicted gene that interacts with BTG, the regulator of the cell cycle, especially in B cells [ 75 ].…”

Efficacy of oral administration of lactic acid bacteria isolated from cocoa in a fermented milk preparation: reduction of colitis in an experimental rat model

“…IBD results from an exaggerated and continuous inflammatory response to resident microbiota in individuals with genetic predisposition (Zemljic et al, 2014). A growing body of data indicates that excessive amounts of cytokines, nitric oxide, and chemokines play a role in the development of intestinal damage by disrupting epithelial cell integrity (Grisham et al, 1990;de Mattos et al, 2015).…”

Matrix metalloproteinases as potential fecal biomarkers for ulcerative colitis – a function beyond their proteolytic activity

“…Chronic CD patients are at an increased risk of developing small-bowel cancer, colon cancer, and colorectal cancer (CRC). [12][13][14] Although the etiology for CD is unknown, recent research suggests that in addition to genetic and environmental factors, imbalance of the gut microbiota also contributes to its development. 15 Commensal bacteria in the host intestine epithelial monolayer are diffused through mucosal layers and are able to perform or aid in multiple important functions such as digestion, metabolizing nutrients, preventing infections caused by invasion of foreign pathogens, and maintaining the homeostasis of mucosal immune system.…”

“…Furthermore, different biological pathways such as autophagy, apoptosis, and necrosis can also play a role in the development and the maintenance of the intestinal bacteria balance in patients with CD. 13 The ulcerations caused by CD can be mediated by different pathways resulting in a large amount of proinflammatory cytokines, chemokines, reactive oxygen radicals, and metalloproteinases, suggesting their participation in the development of the inflammatory response to CD. 15,16 Recent studies suggest that a large range of cell types secreting MMPs during CD reflects a higher correlation to the activity of this form of IBD.…”

“…These microorganisms execute different important cellular functions such as protecting from invading pathogens, assisting in digestion and releasing nutrients, as well as maintaining the colonic immunity. 13 Moreover, gut microbial products also can initiate inflammation as well as regulate immune cells and immune response in colonic epithelium. Hence, the dysregulation of immune response to enteric bacteria induces sustained, overproduction of multiple inflammatory cytokines and reactive oxygen and nitrogen species that directly or indirectly damage colonic tissues, leading to erosions, ulcerations fibrosis, and edema.…”