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The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD)...
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The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 November 2020) | Viewed by 35493

Special Issue Editors

Prof. Dr. Silvio Danese

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Guest Editor
Humanitas University, Milan, Italy
Interests: inflammatory bowel disease; inflammation; gut vascular barrier; immune response; leukocyte trafficking; lipid mediators; colorectal cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Laurent Peyrin-biroulet

grade E-Mail Website
Guest Editor
Department of Gastroenterology, Nancy University Hospital, Université de Lorraine, 54500 Vandoeuvre-lès-Nancy, France
Interests: inflammatory bowel diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia D’Alessio

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Guest Editor
Humanitas University, Via Rita Levi Montalcini 4, Pieve Emanuele, 20090 Milan, Italy
Interests: lymphatic system; gut inflammation; virome; microbiota; resolution of inflammation; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, substantial progress has been made in understanding the pathogenetic mechanisms of inflammatory bowel disease (IBD), specifically Crohn’s disease (CD) and ulcerative colitis (UC). Recent studies have examined the concept that IBD could result from the dysregulation of the intestinal barrier and a pathologic activation of the intestinal immune response toward several bacterial or viral antigens. This has been translated into newer and more effective therapies—biologic and molecular therapies—that have decreased the occurrence of flares, led to remission in more patients, and improved patients’ quality of life.

To date, several factors have been proposed to be involved in the pathogenesis of IBD, including antigen presentation and balance between the different T-cell subpopulations, altered microbiota, anomalies of immune regulation, and phagocytosis; nevertheless, new cellular and molecular targets are under investigation and novel therapeutic approaches have been developed accordingly.

This Special Issue aims to summarize the current knowledge on the cellular and molecular mechanisms behind the pathogenesis of IBD and IBD-related complications, focusing on promising and emerging targets and linking pre-clinical and translational research with clinical studies.

We look forward to your contributions.

Prof. Dr. Silvio Danese
Prof. Laurent Peyrin-biroulet
Dr. Silvia D’Alessio
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • intestinal inflammation
  • immune-mediated disease
  • microbiota
  • leukocyte trafficking
  • pro-and anti-inflammatory mechanisms
  • IBD-related complications

Published Papers (6 papers)

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Research

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20 pages, 1955 KiB  
Article
Probiotic Lactobacillus and Bifidobacterium Strains Counteract Adherent-Invasive Escherichia coli (AIEC) Virulence and Hamper IL-23/Th17 Axis in Ulcerative Colitis, but Not in Crohn’s Disease
by Gabriella Leccese, Alessia Bibi, Stefano Mazza, Federica Facciotti, Flavio Caprioli, Paolo Landini and Moira Paroni
Cells 2020, 9(8), 1824; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9081824 - 01 Aug 2020
Cited by 41 | Viewed by 4875
Abstract
Hypersecretion of proinflammatory cytokines and dysregulated activation of the IL-23/Th17 axis in response to intestinal microbiota dysbiosis are key factors in the pathogenesis of inflammatory bowel diseases (IBD). In this work, we studied how Lactobacillus and Bifidobacterium strains affect AIEC-LF82 virulence mechanisms and [...] Read more.
Hypersecretion of proinflammatory cytokines and dysregulated activation of the IL-23/Th17 axis in response to intestinal microbiota dysbiosis are key factors in the pathogenesis of inflammatory bowel diseases (IBD). In this work, we studied how Lactobacillus and Bifidobacterium strains affect AIEC-LF82 virulence mechanisms and the consequent inflammatory response linked to the CCR6–CCL20 and IL-23/Th17 axes in Crohn’s disease (CD) and ulcerative colitis (UC) patients. All Lactobacillus and Bifidobacterium strains significantly reduced the LF82 adhesion and persistence within HT29 intestinal epithelial cells, inhibiting IL-8 secretion while not affecting the CCR6–CCL20 axis. Moreover, they significantly reduced LF82 survival within macrophages and dendritic cells, reducing the secretion of polarizing cytokines related to the IL-23/Th17 axis, both in healthy donors (HD) and UC patients. In CD patients, however, only B. breve Bbr8 strain was able to slightly reduce the LF82 persistence within dendritic cells, thus hampering the IL-23/Th17 axis. In addition, probiotic strains were able to modulate the AIEC-induced inflammation in HD, reducing TNF-α and increasing IL-10 secretion by macrophages, but failed to do so in IBD patients. Interestingly, the probiotic strains studied in this work were all able to interfere with the IL-23/Th17 axis in UC patients, but not in CD patients. The different interaction mechanisms of probiotic strains with innate immune cells from UC and CD patients compared to HD suggest that testing on CD-derived immune cells may be pivotal for the identification of novel probiotic strains that could be effective also for CD patients. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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15 pages, 1307 KiB  
Article
Molecular Changes in the Non-Inflamed Terminal Ileum of Patients with Ulcerative Colitis
by Ho-Su Lee, Maaike Vancamelbeke, Sare Verstockt, Tom Wilms, Bram Verstockt, João Sabino, Marc Ferrante, Séverine Vermeire and Isabelle Cleynen
Cells 2020, 9(8), 1793; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9081793 - 28 Jul 2020
Cited by 4 | Viewed by 2815
Abstract
Ulcerative colitis is a chronic inflammatory disease confined to the colon. Although the etiopathogenesis remains unknown, small bowel dysfunctions like histological and permeability alterations have been described in ulcerative colitis. We evaluated the molecular gene signature in the non-inflamed terminal ileum of 36 [...] Read more.
Ulcerative colitis is a chronic inflammatory disease confined to the colon. Although the etiopathogenesis remains unknown, small bowel dysfunctions like histological and permeability alterations have been described in ulcerative colitis. We evaluated the molecular gene signature in the non-inflamed terminal ileum of 36 ulcerative colitis patients (7 active, with Mayo endoscopic subscore ≥2, and 29 inactive) as compared to 15 non-inflammatory bowel disease controls. Differential gene expression analysis with DESeq2 showed distinct expression patterns depending on disease activity and maximal disease extent. We found 84 dysregulated genes in patients with active extensive colitis and 20 in inactive extensive colitis, compared to controls. There was an overlap of 5 genes: REG1B, REG1A, MUC4, GRAMD2, and CASP10. In patients with left-sided colitis, ileal gene expression levels were similar to controls. Based on gene co-expression analysis, ileal changes in active ulcerative colitis patients were related to immune functions. The ileal changes in the inactive ulcerative colitis subjects converged into the maintenance of the intestinal barrier through increased mitochondrial function and dampened immune functions. In conclusion, we identified molecular changes in the non-inflamed ileum of ulcerative colitis that are dependent on colonic inflammation. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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20 pages, 1946 KiB  
Article
Development of Mucosal PNAd+ and MAdCAM-1+ Venules during Disease Course in Ulcerative Colitis
by Britt Roosenboom, Ellen G. van Lochem, Jos Meijer, Carolijn Smids, Stefan Nierkens, Eelco C. Brand, Liselot W. van Erp, Larissa G.J.M. Kemperman, Marcel J.M. Groenen, Carmen S. Horjus Talabur Horje and Peter J. Wahab
Cells 2020, 9(4), 891; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9040891 - 06 Apr 2020
Cited by 9 | Viewed by 2738
Abstract
PNAd and MAdCAM-1 addressins on venules are of importance in T-cell homing and potential therapeutic targets in ulcerative colitis (UC). Normally, PNAd+ high endothelial venules (HEVs) are only present in lymphoid organs, whereas small numbers of MAdCAM-1+ venules can be seen [...] Read more.
PNAd and MAdCAM-1 addressins on venules are of importance in T-cell homing and potential therapeutic targets in ulcerative colitis (UC). Normally, PNAd+ high endothelial venules (HEVs) are only present in lymphoid organs, whereas small numbers of MAdCAM-1+ venules can be seen in non-lymphoid tissue. We aimed to study their presence in the intestinal mucosa of UC patients at diagnosis and during follow-up, and their correlation with disease activity. Colonic biopsy specimens of 378 UC patients were analyzed by immunohistochemistry for CD3, CD20, ERG, MECA-79 (PNAd) and MECA-376 (MAdCAM-1) and compared to healthy controls (HC). The proportion of PNAd+HEVs in UC at diagnosis was 4.9% (IQR 2.0%–8.3%), while none were detected in HC. During follow-up, PNAd+HEVs completely disappeared in remission (n = 93), whereas the proportion in active disease was similar to baseline (n = 285, p = 0.39). The proportion of MAdCAM-1+venules in UC at baseline was 5.8% (IQR 2.6–10.0). During follow-up, the proportion in remission was comparable to diagnosis, but upregulated (7.5% (IQR 4.4–10.9), p = 0.001) in active disease. In conclusion, PNAd+HEVs appear in UC during active inflammation which could thus serve as a marker for disease activity, whereas MAdCAM-1+venules remain present after inflammation is resolved and increase after subsequent flares, reflecting chronicity and potentially serving as a therapeutic target. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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Review

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18 pages, 1416 KiB  
Review
Interplay between Cellular and Molecular Mechanisms Underlying Inflammatory Bowel Diseases Development—A Focus on Ulcerative Colitis
by Iuliana Samoilă, Sorina Dinescu and Marieta Costache
Cells 2020, 9(7), 1647; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9071647 - 09 Jul 2020
Cited by 27 | Viewed by 5584
Abstract
Inflammatory bowel diseases (IBD) are defined by the continuous inflammation of the gastrointestinal tract. During inflammation, the number of pathogens in the intestinal epithelium increases, leading to inflammasome assembly. Inflammasome activation is meant to protect the intestinal epithelial barrier from further damage by [...] Read more.
Inflammatory bowel diseases (IBD) are defined by the continuous inflammation of the gastrointestinal tract. During inflammation, the number of pathogens in the intestinal epithelium increases, leading to inflammasome assembly. Inflammasome activation is meant to protect the intestinal epithelial barrier from further damage by maintaining homeostasis. Although its purpose is to protect the cells, excessive nucleotide-binding oligomerization domain-like receptor and pyrin domain-containing protein 3 (NLRP3) inflammasome assembly is responsible for the synthesis of a high number of pro-inflammatory cytokines. The activation of two crucial pathways, autophagy process, and unfolded protein response, is initiated for restoring homeostasis. Aberrant expression of miRNAs and lncRNAs also interfere with the pathogenic mechanisms of IBD, as these non-coding transcripts play key roles in regulation of biological processes, such as inflammation and immunity. This review thoroughly describes the cellular and molecular mechanism that trigger and perpetuate inflammation in ulcerative colitis (UC) patients. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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24 pages, 717 KiB  
Review
The Role of Gut Microbiota Biomodulators on Mucosal Immunity and Intestinal Inflammation
by Chiara Amoroso, Federica Perillo, Francesco Strati, Massimo Fantini, Flavio Caprioli and Federica Facciotti
Cells 2020, 9(5), 1234; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9051234 - 16 May 2020
Cited by 119 | Viewed by 11534
Abstract
Alterations of the gut microbiota may cause dysregulated mucosal immune responses leading to the onset of inflammatory bowel diseases (IBD) in genetically susceptible hosts. Restoring immune homeostasis through the normalization of the gut microbiota is now considered a valuable therapeutic approach to treat [...] Read more.
Alterations of the gut microbiota may cause dysregulated mucosal immune responses leading to the onset of inflammatory bowel diseases (IBD) in genetically susceptible hosts. Restoring immune homeostasis through the normalization of the gut microbiota is now considered a valuable therapeutic approach to treat IBD patients. The customization of microbe-targeted therapies, including antibiotics, prebiotics, live biotherapeutics and faecal microbiota transplantation, is therefore considered to support current therapies in IBD management. In this review, we will discuss recent advancements in the understanding of host−microbe interactions in IBD and the basis to promote homeostatic immune responses through microbe-targeted therapies. By considering gut microbiota dysbiosis as a key feature for the establishment of chronic inflammatory events, in the near future it will be suitable to design new cost-effective, physiologic, and patient-oriented therapeutic strategies for the treatment of IBD that can be applied in a personalized manner. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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17 pages, 2929 KiB  
Review
Single-Cell Protein and RNA Expression Analysis of Mononuclear Phagocytes in Intestinal Mucosa and Mesenteric Lymph Nodes of Ulcerative Colitis and Crohn’s Disease Patients
by Laurence Chapuy and Marika Sarfati
Cells 2020, 9(4), 813; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9040813 - 27 Mar 2020
Cited by 9 | Viewed by 7248
Abstract
Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are driven by an abnormal immune response to commensal microbiota in genetically susceptible hosts. In addition to epithelial and stromal cells, innate and adaptive immune systems are both involved in [...] Read more.
Inflammatory bowel diseases (IBDs), which include Crohn’s disease (CD) and ulcerative colitis (UC), are driven by an abnormal immune response to commensal microbiota in genetically susceptible hosts. In addition to epithelial and stromal cells, innate and adaptive immune systems are both involved in IBD immunopathogenesis. Given the advances driven by single-cell technologies, we here reviewed the immune landscape and function of mononuclear phagocytes in inflamed non-lymphoid and lymphoid tissues of CD and UC patients. Immune cell profiling of IBD tissues using scRNA sequencing combined with multi-color cytometry analysis identifies unique clusters of monocyte-like cells, macrophages, and dendritic cells. These clusters reflect either distinct cell lineages (nature), or distinct or intermediate cell types with identical ontogeny, adapting their phenotype and function to the surrounding milieu (nurture and tissue imprinting). These advanced technologies will provide an unprecedented view of immune cell networks in health and disease, and thus may offer a personalized medicine approach to patients with IBD. Full article
(This article belongs to the Special Issue The Molecular and Cellular Basis for Inflammatory Bowel Diseases (IBD) 2020)
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