Abstract
Enteric glial cells (EGC) are known to regulate gastrointestinal functions; however, their role in Crohn’s disease (CD) is elusive. Microscopic erosions over the ileal Peyer’s patches are early signs of CD. The aim of this work was to assess the localization of EGC in the follicle and interfollicular region of the Peyer’s patches and in the lamina propria and study the effects of EGC mediators on barrier function in CD patients and non-inflammatory bowel disease (non-IBD) controls. EGC markers, glial fibrillary acidic protein (GFAP), and S100 calcium-binding protein β (S100β) were quantified by immunofluorescence and Western blotting. Both markers showed significantly more EGC in the Peyer’s patches and lamina propria of CD patients compared to the non-IBD controls. In CD patients there were significantly more EGC in Peyer’s patches compared to lamina propria, while the opposite pattern was seen in controls. Barrier function studies using Ussing chambers showed increased paracellular permeability by EGC mediators in CD patients, whereas permeability decreased by the mediators in controls. We show the accumulation of EGC in Peyer’s patches of CD patients. Moreover, EGC mediators induced barrier dysfunction in CD patients. Thus, EGC might have harmful impacts on ongoing inflammation and contribute to the pathophysiology of the disease.
Highlights
Crohn’s disease (CD) is an inflammatory bowel disease (IBD) with an unknown etiology; it is well established that genetic [1,2], environmental [3], microbial [4], and immunological factors [5] contribute to the disease pathogenesis
We recently showed [10] a higher number of mast cells and an up-regulation of mast cells expressing receptors for vasoactive intestinal polypeptide (VIP) in the Peyer’s patches and interfollicular region (IFR) of patients with CD compared to non-IBD controls
Increased Numbers of EGCGFAP+ in CD Patients Compared to Non-IBD Controls
Summary
Crohn’s disease (CD) is an inflammatory bowel disease (IBD) with an unknown etiology; it is well established that genetic [1,2], environmental [3], microbial [4], and immunological factors [5] contribute to the disease pathogenesis. Covering the Peyer’s patches [6]. The Peyer’s patches are important for immune responses and have been associated with CD pathogenesis [6,7,8]. Peyer’s patches are dome-like structures, consisting of a follicle with a B-cell germinal center surrounded by a T-cell interfollicular region (IFR). Within the Peyer’s patches, there are a variety of immune cells with the region between the FAE and the follicle, the subepithelial dome, being rich in dendritic cells and macrophages [9]. We recently showed [10] a higher number of mast cells and an up-regulation of mast cells expressing receptors for vasoactive intestinal polypeptide (VIP) in the Peyer’s patches and IFR of patients with CD compared to non-IBD controls
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