Abstract
The human gut relies on several cellular and molecular mechanisms to allow for an intact and dynamical intestinal barrier. Normally, only small amounts of luminal content pass the mucosa, however, if the control is broken it can lead to enhanced passage, which might damage the mucosa, leading to pathological conditions, such as inflammatory bowel disease (IBD). It is well established that genetic, environmental, and immunological factors all contribute in the pathogenesis of IBD, and a disturbed intestinal barrier function has become a hallmark of the disease. Genetical studies support the involvement of intestinal barrier as several susceptibility genes for IBD encode proteins with key functions in gut barrier and homeostasis. IBD patients are associated with loss in bacterial diversity and shifts in the microbiota, with a possible link to local inflammation. Furthermore, alterations of immune cells and several neuro-immune signaling pathways in the lamina propria have been demonstrated. An inappropriate immune activation might lead to mucosal inflammation, with elevated secretion of pro-inflammatory cytokines that can affect the epithelium and promote a leakier barrier. This review will focus on the main cells and molecular mechanisms in IBD and how these can be targeted in order to improve intestinal barrier function and reduce inflammation.
Highlights
Inflammatory bowel disease (IBD), mainly comprised of ulcerative colitis and Crohn’s disease, is characterized by symptoms such as abdominal pain, diarrhea, and weight loss
T regulatory (Treg) cells are a subset of T cells able to suppress the activation and effector function of several immune cells involved in intestinal inflammation
It is known that the numbers of activated eosinophils are higher in patients with active and inactive ulcerative colitis compared with controls, and interestingly, the amount of eosinophils has been shown to be higher in the inactive mucosa compared to the mucosa with an active inflammation [108]
Summary
Inflammatory bowel disease (IBD), mainly comprised of ulcerative colitis and Crohn’s disease, is characterized by symptoms such as abdominal pain, diarrhea, and weight loss. The ability of Fusobacterium species to invade the intestinal epithelium increase with the severity immune cells and neuroimmune signaling pathways in the lamina propria This might give rise to an of IBD [9], indicating that these strains may play a role in IBD pathogenesis. Inappropriate immune activation that can lead to mucosal inflammation, with elevated secretion of Except from an intestinal dysbiosis, patients with IBD have shown to have alterations in several pro-inflammatory cytokines that insignaling turn willpathways affect the andThis promote leaky immune cells and neuroimmune in epithelial the laminacells propria. Current and potential therapies have been developed in order to reduce inflammation and improve intestinal barrier function
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