scholarly journals The Role of Extracellular Matrix Components in Inflammatory Bowel Diseases

2021 ◽  
Vol 10 (5) ◽  
pp. 1122
Author(s):  
Alicja Derkacz ◽  
Paweł Olczyk ◽  
Krystyna Olczyk ◽  
Katarzyna Komosinska-Vassev
Keyword(s):  
Extracellular Matrix ◽  
Inflammatory Bowel Diseases ◽  
Healing Process ◽  
Immunological Response ◽  
Matrix Remodeling ◽  
Ecm Remodeling ◽  
Intestinal Fibrosis ◽  
Extracellular Matrix Components ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The remodeling of extracellular matrix (ECM) within the intestine tissues, which simultaneously involves an increased degradation of ECM components and excessive intestinal fibrosis, is a defining trait of the progression of inflammatory bowel diseases (IBDs), which include ulcerative colitis (UC) and Crohn’s disease (CD). The increased activity of proteases, especially matrix metalloproteinases (MMPs), leads to excessive degradation of the extracellular matrix and the release of protein and glycoprotein fragments, previously joined with the extracellular matrix, into the circulation. MMPs participate in regulating the functions of the epithelial barrier, the immunological response, and the process of wound healing or intestinal fibrosis. At a later stage of fibrosis during IBD, excessive formation and deposition of the matrix is observed. To assess changes in the extracellular matrix, quantitative measurement of the concentration in the blood of markers dependent on the activity of proteases, involved in the breakdown of extracellular matrix proteins as well as markers indicating the formation of a new ECM, has recently been proposed. This paper describes attempts to use the quantification of ECM components as markers to predict intestinal fibrosis and evaluate the healing process of the gut. The markers which reflect increased ECM degradation, together with the ones which show the process of creating a new matrix during IBD, allow the attainment of important information regarding the changes in the intestinal tissue, epithelial integrity and extracellular matrix remodeling. This paper contains evidence confirming that ECM remodeling is an integral part of directional cell signaling in the progression of IBD, and not only a basis for the ongoing processes.

scholarly journals Immunotherapeutic Effects of β-D Mannuronic Acid on IL-4, GATA3, IL-17 and RORC Gene Expression in the PBMC of Patients with Inflammatory Bowel Diseases

2018 ◽  
Author(s):  
Hussaini Alhassan Mohammed ◽  
Ali Akbar Saboor-Yaraghi ◽  
Homayoun Vahedi ◽  
Ghordratollah Panahi ◽  
Gholamreza Hemmasi ◽  
...  
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Immunological Response ◽  
Quantitative Real Time Pcr ◽  
Mannuronic Acid ◽  
Immune Mediated ◽  
Genes Expression ◽  
Bowel Diseases ◽  
Research Findings ◽  
Inflammatory Bowel ◽  
Normal Controls

Inflammatory bowel diseases (IBD) are chronic relapsing immune-mediated disorders that result from an aberrant immunological response. IBD comprises of Crohn's disease (CD) and ulcerative colitis (UC). The precise aetiology of IBD has not been fully understood, however, recent studies support the hypothesis that patients with IBD have a dysregulated immune response to endogenous bacteria in the gastrointestinal tract (GIT). The increasing number of hospitalisation coupled with the high economic burden faced by IBD patients, calls for more concerted research efforts, to design a potent and credible treatment option for these strata of patients. This research was designed to test the efficacy and potency of β-D Mannuronic acid (M2000) in the treatment of IBD. Ten ml of blood was aseptically collected from 24 IBD patients and 24 normal controls. PBMC was isolated and stimulated with 1 µg/mL of LPS and incubated for 4 hours. The cells were later treated with 10 µg/mL or 50 µg/mL of Mannuronic acid and incubated for 24 hours at 370C under 5% CO2 and 100% humidity. After the incubation, RNA was extracted from the cells, cDNA was synthesised, and the expression of the gene was evaluated using quantitative real-time PCR. The result indicated a significant down-regulation of RORC and IL-17 genes expression, while the expression of IL-4 and GATA3 genes were significantly up-regulated. These research findings have shown that M2000 a biocompatible agent, that has an immunotherapeutic, immunomodulatory and immunosuppressive effects on the PBMC of IBD patients.

scholarly journals The Diagnostic Usefulness of Circulating Profile of Extracellular Matrix Components: Sulfated Glycosaminoglycans (sGAG), Hyaluronan (HA) and Extracellular Part of Syndecan-1 (sCD138) in Patients with Crohn’s Disease and Ulcerative Colitis

2021 ◽  
Vol 10 (8) ◽  
pp. 1722
Author(s):  
Alicja Derkacz ◽  
Paweł Olczyk ◽  
Agnieszka Jura-Półtorak ◽  
Krystyna Olczyk ◽  
Katarzyna Komosinska-Vassev
Keyword(s):  
Ulcerative Colitis ◽  
Extracellular Matrix ◽  
Ecm Remodeling ◽  
Mayo Score ◽  
Extracellular Matrix Components ◽  
Adalimumab Therapy ◽  
Bowel Diseases ◽  
Diagnostic Usefulness ◽  
Quantitative Changes ◽  
One Year

The described research focused on the diagnostic usefulness of sulfated glycosaminoglycans (sGAG), hyaluronan (HA), and extracellular part of syndecan-1 (sCD138) as new markers related to extracellular matrix (ECM) remodeling in the intestine during the two most common forms of inflammatory bowel diseases (IBD), i.e., ulcerative colitis (UC) and Crohn’ disease (CD). Inflammatory markers belonging to ECM components were assessed in serum of patients with IBD using an immunoenzymatic method (HA and sCD138) and a method based on the reaction with dimethylmethylene blue (sulfated GAG). Measurements were carried out twice: at baseline and after one year of therapy with prednisone (patients with CD) or adalimumab (patients with UC). No quantitative changes were observed in serum sGAG, HA, and sCD138 concentrations between patients newly diagnosed with CD and the healthy group. In the case of patients with UC, the parameter which significantly differentiated healthy subjects and patients with IBD before biological therapy was HA. Significant correlation between serum HA level and inflammation activity, expressed as Mayo score, was also observed in patients with UC. Moreover, the obtained results have confirmed that steroid therapy with prednisone significantly influenced the circulating profile of all examined ECM components (sGAG, HA, and sCD138), whereas adalimumab therapy in patients with UC led to a significant change in only circulating sGAG levels. Moreover, the significant differences in serum HA levels between patients with UC and CD indicate that quantification of circulating HA may be useful in the differential diagnosis of CD and UC.

scholarly journals Prebiotics, Probiotics, Synbiotics, Paraprobiotics and Postbiotic Compounds in IBD

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1903
Author(s):  
Adrian Martyniak ◽  
Aleksandra Medyńska-Przęczek ◽  
Andrzej Wędrychowicz ◽  
Szymon Skoczeń ◽  
Przemysław J. Tomasik
Keyword(s):  
Intestinal Microbiota ◽  
Inflammatory Bowel Diseases ◽  
Gut Microbiome ◽  
Immunological Response ◽  
Bacterial Metabolism ◽  
Dietary Fibers ◽  
Beneficial Bacteria ◽  
New Methods ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The increasing incidence of inflammatory bowel diseases (IBD) and the increasing severity of the course of these diseases create the need for developing new methods of therapy. The gut microbiome is extensively studied as a factor influencing the development and course of IBD. The composition of intestinal microbiota can be relatively easily modified by diet (i.e., prebiotics, mainly dietary fibers) and bacterial supplementation using beneficial bacteria strains called probiotics. Additionally, the effects of the improved microbiome could be enhanced or gained by using paraprobiotics (non-viable, inactivated bacteria or their components) and/or postbiotics (products of bacterial metabolism or equal synthetic products that beneficially modulate immunological response and inflammation). This study summarizes the recent works on prebiotics, probiotics, synbiotics (products merging pre- and probiotics), paraprobiotics and postbiotics in IBD.

scholarly journals Intestinal fibrosis: The Achilles heel of inflammatory bowel diseases?

2020 ◽  
Vol 21 (6) ◽  
pp. 306-307 ◽  
Author(s):  
Ren Mao ◽  
Jordi Rimola ◽  
Min‐Hu Chen ◽  
Florian Rieder
Keyword(s):  
Inflammatory Bowel Diseases ◽  
Intestinal Fibrosis ◽  
Bowel Diseases ◽  
Inflammatory Bowel

scholarly journals The Multiple Faces of Integrin–ECM Interactions in Inflammatory Bowel Disease

2021 ◽  
Vol 22 (19) ◽  
pp. 10439
Author(s):  
Valentina Garlatti ◽  
Sara Lovisa ◽  
Silvio Danese ◽  
Stefania Vetrano
Keyword(s):  
Inflammatory Bowel Disease ◽  
Extracellular Matrix ◽  
Bowel Disease ◽  
Great Promise ◽  
Matrix Remodeling ◽  
Independent Manner ◽  
Damage Site ◽  
Intestinal Fibrosis ◽  
Inflammatory Bowel

Inflammatory Bowel Disease (IBD) comprises a series of chronic and relapsing intestinal diseases, with Crohn’s disease and ulcerative colitis being the most common. The abundant and uncontrolled deposition of extracellular matrix, namely fibrosis, is one of the major hallmarks of IBD and is responsible for the progressive narrowing and closure of the intestine, defined as stenosis. Although fibrosis is usually considered the product of chronic inflammation, the substantial failure of anti-inflammatory therapies to target and reduce fibrosis in IBD suggests that fibrosis might be sustained in an inflammation-independent manner. Pharmacological therapies targeting integrins have recently shown great promise in the treatment of IBD. The efficacy of these therapies mainly relies on their capacity to target the integrin-mediated recruitment and functionality of the immune cells at the damage site. However, by nature, integrins also act as mechanosensitive molecules involved in the intracellular transduction of signals and modifications originating from the extracellular matrix. Therefore, understanding integrin signaling in the context of IBD may offer important insights into mechanisms of matrix remodeling, which are uncoupled from inflammation and could underlie the onset and persistency of intestinal fibrosis. In this review, we present the currently available knowledge on the role of integrins in the etiopathogenesis of IBD, highlighting their role in the context of immune-dependent and independent mechanisms.

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