Role of vitamin D derivatives in intestinal tissue of patients with inflammatory bowel diseases

Martinesi, Maria; Ambrosini, Stefano; Treves, Cristina; Züegel, Ulrich; Steinmeyer, Andreas; Annese, Vito; Milla, Mónica; Bonanomi, Andrea; Stio, Maria

doi:10.1016/j.crohns.2014.02.005

Cited by 9 publications

(3 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, recent studies in IBD patients demonstrated that an increase of epithelial permeability precedes flares of inflammatory bowel pointing towards a causative role of epithelial barrier breakdown in the development of intestinal inflammation ( 35 , 56 – 58 ). The latter is supported by reports that a decrease of epithelial permeability by application of vitamin D ( 59 , 60 ), probiotics ( 61 – 63 ), IL-22-triggered mucus production ( 64 ), butyrate ( 65 , 66 ), or an anti-TNF antibody caused clinical amelioration of chronic colitis ( 67 , 68 ). Moreover, alternative portals for gut leakiness such as brush border functions and intestinal bacterial endocytosis by epithelial cells have to be considered and may play important pathogenic roles providing putative targets for therapy of inflammatory bowel disease ( 15 ).…”

Section: Structure and Function Of The Epithelial Barrier In Ibdmentioning

confidence: 74%

Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease

2021

View full text Add to dashboard Cite

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.

show abstract

Section: Structure and Function Of The Epithelial Barrier In Ibdmentioning

confidence: 74%

Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease

2021

View full text Add to dashboard Cite

show abstract

“…ZK191784 is an intestine specific vitamin D analogue which can exert an anti-inflammatory effect without causing hypercalcaemia [ 168 – 170 ]. This compound and calcitriol were tested in cultured colon biopsies of healthy and IBD patients and were found to reduce MMP-2, -3, and -9 levels as well as the adhesion molecules ICAM-1 and MAdCAM-1 [ 171 ].…”

Section: Mmp Inhibitionmentioning

confidence: 99%

Matrix Metalloproteinases in Inflammatory Bowel Disease: An Update

O'Sullivan

Gilmer

Medina

2015

Mediators of Inflammation

134

119

View full text Add to dashboard Cite

Matrix metalloproteinases (MMPs) are known to be upregulated in inflammatory bowel disease (IBD) and other inflammatory conditions, but while their involvement is clear, their role in many settings has yet to be determined. Studies of the involvement of MMPs in IBD since 2006 have revealed an array of immune and stromal cells which release the proteases in response to inflammatory cytokines and growth factors. Through digestion of the extracellular matrix and cleavage of bioactive proteins, a huge diversity of roles have been revealed for the MMPs in IBD, where they have been shown to regulate epithelial barrier function, immune response, angiogenesis, fibrosis, and wound healing. For this reason, MMPs have been recognised as potential biomarkers for disease activity in IBD and inhibition remains a huge area of interest. This review describes new roles of MMPs in the pathophysiology of IBD and suggests future directions for the development of treatment strategies in this condition.

show abstract

“…Accordingly, new therapy strategies based on epithelial restoration led to promising results in IBD patients. For instance, therapeutically induced decrease of epithelial permeability by vitamin D (65, 66) or probiotics (67–69), IL-22-triggered mucus production (70) or maintenance of epithelial cell integrity by butyrate (71, 72), or anti-TNF antibody treatment resulted in a clinical amelioration of chronic colitis (73, 74). The remaining open question is which mechanism might regulate cytoskeleton remodeling and epithelial permeability.…”

Section: Epithelial Barrier Regulation During Intestinal Inflammationmentioning

confidence: 99%

Interplay of GTPases and Cytoskeleton in Cellular Barrier Defects during Gut Inflammation

2017

View full text Add to dashboard Cite

An essential role of the intestine is to build and maintain a barrier preventing the luminal gut microbiota from invading the host. This involves two coordinated physical and immunological barriers formed by single layers of intestinal epithelial and endothelial cells, which avoid the activation of local immune responses or the systemic dissemination of microbial agents, and preserve tissue homeostasis. Accordingly, alterations of epithelial and endothelial barrier functions have been associated with gut inflammation, for example during inflammatory bowel disease (IBD). The discriminative control of nutriment uptake and sealing toward potentially pathological microorganisms requires a profound regulation of para- and transcellular permeability. On the subcellular level, the cytoskeleton exerts key regulatory functions in the maintenance of cellular barriers. Increased epithelial/endothelial permeability occurs primarily as a result of a reorganization of cytoskeletal–junctional complexes. Pro-inflammatory mediators such as cytokines can induce cytoskeletal rearrangements, causing inflammation-dependent defects in gut barrier function. In this context, small GTPases of the Rho family and large GTPases from the Dynamin superfamily appear as major cellular switches regulating the interaction between intercellular junctions and actomyosin complexes, and in turn cytoskeleton plasticity. Strikingly, some of these proteins, such as RhoA or guanylate-binding protein-1 (GBP-1) have been associated with gut inflammation and IBD. In this review, we will summarize the role of small and large GTPases for cytoskeleton plasticity and epithelial/endothelial barrier in the context of gut inflammation.

show abstract

Role of vitamin D derivatives in intestinal tissue of patients with inflammatory bowel diseases

Abstract: Based on the increased expression of ICAM-1, MAdCAM-1 and MMP-2,-9,-3 in IBD, our study suggests that vitamin D derivatives may be effective in the management of these diseases.

Cited by 9 publications

References 52 publications

Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease

Angiocrine Regulation of Epithelial Barrier Integrity in Inflammatory Bowel Disease

Matrix Metalloproteinases in Inflammatory Bowel Disease: An Update

Interplay of GTPases and Cytoskeleton in Cellular Barrier Defects during Gut Inflammation

Contact Info

Product

Resources

About