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Pathophysiology and Treatment of Inflammatory Bowel Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 10321

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Special Issue Editors

Dr. Frédérick Barreau

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Guest Editor

INSERM, INRAE, ENVT, Université de Toulouse, UPS, F-31000 Toulouse, France
Interests: intestinal barrier function; gut microbiota; mucosal immunology; inflammatory bowel disease; IBD pathways (Nod2, autophagy, endoplasmic reticulum stress, Th17)
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Emmanuel Mas

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Guest Editor

1. INSERM, INRAE, ENVT, Université de Toulouse, UPS, F-31000 Toulouse, France
2. Unité de Gastroentérologie, Hépatologie, Nutrition, Diabétologie et Maladies Héréditaires du Métabolisme, Hôpital des Enfants, CHU de Toulouse, F-31300 Toulouse, France
Interests: inflammatory bowel disease; translational research; nutrition; cystic fibrosis; intestinal polyposis; endoscopy; gut microbiota
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Crohn’s disease (CD) and ulcerative colitis (UC), the two main subtypes of inflammatory bowel disease (IBD), are chronic relapsing inflammatory disorders of the gastrointestinal tract. Although the etiology of IBD is poorly understood, IBD are complex diseases involving genetic and environmental factors. The pathophysiology of IBD is described to result from an abnormal crosstalk between gut microbiota and immune system favored by a weakened intestinal barrier, leading to inflammation. Although the primum movens remains unknown, an increased intestinal permeability is clearly involved in the genesis of this abnormal crosstalk, leading to whole tissue inflammation. Thus, as newly reported intestinal permeability is a sensitive prognostic indicator of relapse in patients with quiescent IBD.

The genetic and environmental factors as well as their interactions involved in IBD pathogenesis are continuously being investigated, and this improved knowledge is contributing to the development of new therapies.

Here, we invite experts to contribute to this Special Issue with original research or review articles investigating the cellular and molecular mechanisms involved in the pathophysiology of IBD, as well as new advances in the therapeutic ways to treat IBD.

Dr. Frédérick Barreau
Prof. Dr. Emmanuel Mas
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

microbiota dysbiosis
microbiota metabolites having anti-inflammatory properties
mucus layer
intestinal permeability
intestinal stem cells
advances on the environmental factors
new advances in the mechanisms by which IBD pathways (Nod2, autophagy, endoplasmic reticulum stress, Th17) alter the homeostasis of the intestinal mucosa

Published Papers (4 papers)

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Research

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14 pages, 2531 KiB

Open AccessArticle

Impact of IBD-Associated Dysbiosis on Bacterial Quorum Sensing Mediated by Acyl-Homoserine Lactone in Human Gut Microbiota

by Nathan Grellier, Marcelino T. Suzuki, Loic Brot, Alice M. S. Rodrigues, Lydie Humbert, Karine Escoubeyrou, Dominique Rainteau, Jean-Pierre Grill, Raphaël Lami and Philippe Seksik

Int. J. Mol. Sci. 2022, 23(23), 15404; https://doi.org/10.3390/ijms232315404 - 6 Dec 2022

Cited by 6 | Viewed by 1868

Abstract

Intestinal dysbiosis is a key feature in the pathogenesis of inflammatory bowel disease (IBD). Acyl-homoserine lactones (AHL) are bacterial quorum-sensing metabolites that may play a role in the changes in host cells-gut microbiota interaction observed during IBD. The objective of our study was to investigate the presence and expression of AHL synthases and receptor genes in the human gut ecosystem during IBD. We used an in silico approach, applied to the Inflammatory Bowel Disease Multi’omics Database comprising bacterial metagenomic and metatranscriptomic data from stools of patients with Crohn’s disease (CD) (n = 50), ulcerative colitis (UC) (n = 27) and non-IBD controls (n = 26). No known putative AHL synthase gene was identified; however, several putative luxR receptors were observed. Regarding the expression of these receptor genes, the luxR gene from Bacteroides dorei was under-expressed in IBD patients (p = 0.02) compared to non-IBD patients, especially in CD patients (p = 0.02). In the dysbiosis situation, one luxR receptor gene from Bacteroides fragilis appeared to be over-expressed (p = 0.04) compared to that of non-dysbiotic patients. Targeting LuxR receptors of bacterial quorum sensing might represent a new approach to modulate the gut microbiota in IBD. Full article

(This article belongs to the Special Issue Pathophysiology and Treatment of Inflammatory Bowel Disease)

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16 pages, 4158 KiB

Open AccessArticle

Presume Why Probiotics May Not Provide Protection in Inflammatory Bowel Disease through an Azoxymethane and Dextran Sodium Sulfate Murine Model

by Ming-Luen Hu, Wei-Shiung Lian, Feng-Sheng Wang, Chao-Hui Yang, Wan-Ting Huang, Jing-Wen Yang, I-Ya Chen and Ming-Yu Yang

Int. J. Mol. Sci. 2022, 23(17), 9689; https://doi.org/10.3390/ijms23179689 - 26 Aug 2022

Cited by 2 | Viewed by 1960

Abstract

Recent studies have shown dysbiosis is associated with inflammatory bowel disease (IBD). However, trying to restore microbial diversity via fecal microbiota transplantation (FMT) or probiotic intervention fails to achieve clinical benefit in IBD patients. We performed a probiotic intervention on a simulated IBD murine model to clarify their relationship. IBD was simulated by the protocol of azoxymethane and dextran sodium sulfate (AOM/DSS) to set up a colitis and colitis-associated neoplasm model on BALB/c mice. A single probiotic intervention using Clostridium butyricum Miyairi (CBM) on AOM/DSS mice to clarify the role of probiotic in colitis, colitis-associated neoplasm, gut microbiota, and immune cytokines was performed. We found dysbiosis occurred in AOM/DSS mice. The CBM intervention on AOM/DSS mice failed to improve colitis and colitis-associated neoplasms but changed microbial composition and unexpectedly increased expression of proinflammatory IL-17A in rectal tissue. We hypothesized that the probiotic intervention caused dysbiosis. To clarify the result, we performed inverse FMT using feces from AOM/DSS mice to normal recipients to validate the pathogenic effect of dysbiosis from AOM/DSS mice and found mice on inverse FMT did develop colitis and colon neoplasms. We presumed the probiotic intervention to some extent caused dysbiosis as inverse FMT. The role of probiotics in IBD requires further elucidation. Full article

(This article belongs to the Special Issue Pathophysiology and Treatment of Inflammatory Bowel Disease)

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16 pages, 6769 KiB

Open AccessArticle

A Preclinical Validation of Iron Oxide Nanoparticles for Treatment of Perianal Fistulizing Crohn’s Disease

by Antoine Cazelles, Maxime K. Collard, Yoann Lalatonne, Sabrina Doblas, Magaly Zappa, Camélia Labiad, Dominique Cazals-Hatem, Léon Maggiori, Xavier Treton, Yves Panis, Ulrich Jarry, Thomas Desvallées, Pierre-Antoine Eliat, Raphaël Pineau, Laurence Motte, Didier Letourneur, Teresa Simon-Yarza and Eric Ogier-Denis

Int. J. Mol. Sci. 2022, 23(15), 8324; https://doi.org/10.3390/ijms23158324 - 28 Jul 2022

Cited by 1 | Viewed by 2556

Abstract

Fistulizing anoperineal lesions are severe complications of Crohn’s disease (CD) that affect quality of life with a long-term risk of anal sphincter destruction, incontinence, permanent stoma, and anal cancer. Despite several surgical procedures, they relapse in about two-thirds of patients, mandating innovative treatments. Ultrasmall particles of iron oxide (USPIO) have been described to achieve in vivo rapid healing of deep wounds in the skin and liver of rats thanks to their nanobridging capability that could be adapted to fistula treatment. Our main purpose was to highlight preclinical data with USPIO for the treatment of perianal fistulizing CD. Twenty male Sprague Dawley rats with severe 2,4,6-trinitrobenzenesulfonic acid solution (TNBS)-induced proctitis were operated to generate two perianal fistulas per rat. At day 35, two inflammatory fistulas were obtained per rat and perineal magnetic resonance imaging (MRI) was performed. After a baseline MRI, a fistula tract was randomly drawn and topically treated either with saline or with USPIO for 1 min (n = 17 for each). The rats underwent a perineal MRI on postoperative days (POD) 1, 4, and 7 and were sacrificed for pathological examination. The primary outcome was the filling or closure of the fistula tract, including the external or internal openings. USPIO treatment allowed the closure and/or filling of all the treated fistulas from its application until POD 7 in comparison with the control fistulas (23%). The treatment with USPIO was safe, permanently closed the fistula along its entire length, including internal and external orifices, and paved new avenues for the treatment of perianal fistulizing Crohn’s disease. Full article

(This article belongs to the Special Issue Pathophysiology and Treatment of Inflammatory Bowel Disease)

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Review

Jump to: Research

32 pages, 1200 KiB

Open AccessReview

Mesenchymal (Stem) Stromal Cells Based as New Therapeutic Alternative in Inflammatory Bowel Disease: Basic Mechanisms, Experimental and Clinical Evidence, and Challenges

by Noemi Eiro, Maria Fraile, Alberto González-Jubete, Luis O. González and Francisco J. Vizoso

Int. J. Mol. Sci. 2022, 23(16), 8905; https://doi.org/10.3390/ijms23168905 - 10 Aug 2022

Cited by 18 | Viewed by 3305

Abstract

Inflammatory bowel diseases (IBD) are an example of chronic diseases affecting 40% of the population, which involved tissue damage and an inflammatory process not satisfactorily controlled with current therapies. Data suggest that mesenchymal stem cells (MSC) may be a therapeutic option for these processes, and especially for IBD, due to their multifactorial approaches such as anti-inflammatory, anti-oxidative stress, anti-apoptotic, anti-fibrotic, regenerative, angiogenic, anti-tumor, or anti-microbial. However, MSC therapy is associated with important limitations as safety issues, handling difficulties for therapeutic purposes, and high economic cost. MSC-derived secretome products (conditioned medium or extracellular vesicles) are therefore a therapeutic option in IBD as they exhibit similar effects to their parent cells and avoid the issues of cell therapy. In this review, we proposed further studies to choose the ideal tissue source of MSC to treat IBD, the implementation of new standardized production strategies, quality controls and the integration of other technologies, such as hydrogels, which may improve the therapeutic effects of derived-MSC secretome products in IBD. Full article

(This article belongs to the Special Issue Pathophysiology and Treatment of Inflammatory Bowel Disease)

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