scholarly journals Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Michael Stürzl ◽  
Meik Kunz ◽  
Susanne M. Krug ◽  
Elisabeth Naschberger
Keyword(s):  
Inflammatory Bowel Disease ◽  
Endothelial Cells ◽  
Blood Vessels ◽  
Bowel Disease ◽  
Epithelial Barrier ◽  
Portal Circulation ◽  
Major Step ◽  
Endothelial Barriers ◽  
Inflammatory Bowel ◽  
Additional Barrier

Inflammatory bowel disease describes chronic inflammatory disorders. The incidence of the disease is rising. A major step in disease development is the breakdown of the epithelial cell barrier. Numerous blood vessels are directly located underneath this barrier. Diseased tissues are heavily vascularized and blood vessels significantly contribute to disease progression. The gut-vascular barrier (GVB) is an additional barrier controlling the entry of substances into the portal circulation and to the liver after passing the first epithelial barrier. The presence of the GVB rises the question, whether the vascular and endothelial barriers may communicate bi-directionally in the regulation of selective barrier permeability. Communication from epithelial to endothelial cells is well-accepted. In contrast, little is known on the respective backwards communication. Only recently, perfusion-independent angiocrine functions of endothelial cells were recognized in a way that endothelial cells release specific soluble factors that may directly act on the epithelial barrier. This review discusses the putative involvement of angiocrine inter-barrier communication in the pathogenesis of IBD.

Serum immunoglobulin G reactive with endothelial cells in inflammatory bowel disease

1994 ◽  
Vol 39 (9) ◽  
pp. 1909-1917 ◽  
Author(s):  
A. M. Sawyerr ◽  
B. E. Pottinger ◽  
C. O. Savage ◽  
N. J. Bradley ◽  
M. Hudson ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Endothelial Cells ◽  
Immunoglobulin G ◽  
Bowel Disease ◽  
Serum Immunoglobulin ◽  
Inflammatory Bowel

Expanding Contributions of Monogenic Very Early Onset Inflammatory Bowel Disease

2021 ◽  
Author(s):  
Jodie Ouahed
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Early Onset ◽  
Current Issue ◽  
Epithelial Barrier ◽  
Mevalonate Kinase Deficiency ◽  
Bowel Diseases ◽  
Life Threatening ◽  
Mucosal Homeostasis ◽  
Inflammatory Bowel

Abstract Currently over 70 genes known to be causative in very early onset inflammatory bowel disease (VEOIBD) have been identified. In the current issue of Inflammatory Bowel Diseases, 2 articles describing monogenetic forms of VEOIBD are highlighted. One describes a patient with life-threatening VEOIBD and a mutation in ITGA6, illustrating the importance of the epithelial barrier in maintaining mucosal homeostasis. The other describes the presentation and management of 10 patients with VEOIBD secondary to damaging mutations in MVK, resulting in mevalonate kinase deficiency. Though most monogenic causes of VEOIBD remain “private,” understanding the different categories of pathways affected in children with VEOIBD is critical and has already resulted in invaluable insight in the management of patients with VEOIBD and may hold strong implications for the care of IBD overall.

scholarly journals Increase in Epithelial Permeability and Cell Metabolism by High Mobility Group Box 1, Inflammatory Cytokines and TPEN in Caco-2 Cells as a Novel Model of Inflammatory Bowel Disease

2020 ◽  
Vol 21 (22) ◽  
pp. 8434
Author(s):  
Maki Miyakawa ◽  
Takumi Konno ◽  
Takayuki Kohno ◽  
Shin Kikuchi ◽  
Hiroki Tanaka ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Growth Factor ◽  
Inflammatory Cytokines ◽  
Zinc Deficiency ◽  
Bowel Disease ◽  
Kinase Inhibitor ◽  
Cell Metabolism ◽  
High Mobility ◽  
Epithelial Barrier ◽  
Inflammatory Bowel

High mobility group box 1 protein (HMGB1) is involved in the pathogenesis of inflammatory bowel disease (IBD). Patients with IBD develop zinc deficiency. However, the detailed roles of HMGB1 and zinc deficiency in the intestinal epithelial barrier and cellular metabolism of IBD remain unknown. In the present study, Caco-2 cells in 2D culture and 2.5D Matrigel culture were pretreated with transforming growth factor-β (TGF-β) type 1 receptor kinase inhibitor EW-7197, epidermal growth factor receptor (EGFR) kinase inhibitor AG-1478 and a TNFα antibody before treatment with HMGB1 and inflammatory cytokines (TNFα and IFNγ). EW-7197, AG-1478 and the TNFα antibody prevented hyperpermeability induced by HMGB1 and inflammatory cytokines in 2.5D culture. HMGB1 affected cilia formation in 2.5D culture. EW-7197, AG-1478 and the TNFα antibody prevented the increase in cell metabolism induced by HMGB1 and inflammatory cytokines in 2D culture. Furthermore, ZnSO4 prevented the hyperpermeability induced by zinc chelator TPEN in 2.5D culture. ZnSO4 and TPEN induced cellular metabolism in 2D culture. The disruption of the epithelial barrier induced by HMGB1 and inflammatory cytokines contributed to TGF-β/EGF signaling in Caco-2 cells. The TNFα antibody and ZnSO4 as well as EW-7197 and AG-1478 may have potential for use in therapy for IBD.

scholarly journals Tumour Necrosis Factor Superfamily Members in the Pathogenesis of Inflammatory Bowel Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Tomasz J. Ślebioda ◽  
Zbigniew Kmieć
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumour Necrosis Factor ◽  
Bowel Disease ◽  
Tumour Necrosis ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Conditions ◽  
Inflammatory Bowel ◽  
Necrosis Factor

Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the gastrointestinal tract of unclear aetiology of which two major forms are Crohn’s disease (CD) and ulcerative colitis (UC). CD and UC are immunologically distinct, although they both result from hyperactivation of proinflammatory pathways in intestines and disruption of intestinal epithelial barrier. Members of the tumour necrosis factor superfamily (TNFSF) are molecules of broad spectrum of activity, including direct disruption of intestinal epithelial barrier integrity and costimulation of proinflammatory functions of lymphocytes. Tumour necrosis factor (TNF) has a well-established pathological role in IBD which also serves as a target in IBD treatment. In this review we discuss the role of TNF and other TNFSF members, notably, TL1A, FasL, LIGHT, TRAIL, and TWEAK, in the pathogenesis of IBD.

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