Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.9
5.1
Journals
Cells
Special Issues
Cellular and Molecular Mechanisms of Inflammatory Bowel Disease
share announcement

Cellular and Molecular Mechanisms of Inflammatory Bowel Disease

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

Deadline for manuscript submissions: closed (10 December 2021) | Viewed by 13057

Special Issue Editor

Dr. Stefano Fiorucci

E-Mail Website
Guest Editor
Department of Surgical and Biomedical Sciences, Section of Gastroenterology, University of Perugia, 06123 Perugia, PG, Italy
Interests: inflammation; inflammatory bowel diseases; innate immunity; bile acids; intestinal microbiota; liver steatosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is my pleasure to invite submissions for the Cells' Special Issue dedicated to inflammatory bowel disease (IBD). IBD is a family of immune-mediated disorders showing an increasing prevalence worldwide. The pathogenesis of IBD is multifactorial and includes genetic factors, as well as a dysfunctional communication between the intestinal microbiota and the immune system, leading to a loss of immunotolerance and to the recruitment of inflammatory cells in to the intestinal mucosa. Both a dysregulated innate and adaptive immunity take part in the pathogenesis of intestinal damage, and multiple cytokines, chemokines, adhesion molecules, and receptors have been shown to take part in the pathogenesis of IBD. Accordingly, multiple therapeutic approaches have been developed. Nevertheless, therapy for IBD remains suboptimal. The present call is designed to accommodate every aspect of IBD from animal models, cellular and molecular mechanisms, intestinal microbiota, basic immunology, biochemistry and signaling mechanisms including original papers and reviews.

Prof. Stefano Fiorucci
Guest Editor

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.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 4798 KiB  
Article
Dynamic, Transient, and Robust Increase in the Innervation of the Inflamed Mucosa in Inflammatory Bowel Diseases
by Miguel Gonzalez Acera, Marvin Bubeck, Fabrizio Mascia, Leonard Diemand, Gregor Sturm, Anja A. Kühl, Raja Atreya, Dieter Chichung Lie, Markus F. Neurath, Michael Schumann, Christoph S.N. Klose, Zlatko Trajanoski, Christoph Becker and Jay V. Patankar
Cells 2021, 10(9), 2253; https://doi.org/10.3390/cells10092253 - 30 Aug 2021
Cited by 5 | Viewed by 3300
Abstract
Inflammatory bowel diseases (IBD) are characterized by chronic dysregulation of immune homeostasis, epithelial demise, immune cell activation, and microbial translocation. Each of these processes leads to proinflammatory changes via the release of cytokines, damage-associated molecular patterns (DAMPs), and pathogen-associated molecular patterns (PAMPs), respectively. [...] Read more.
Inflammatory bowel diseases (IBD) are characterized by chronic dysregulation of immune homeostasis, epithelial demise, immune cell activation, and microbial translocation. Each of these processes leads to proinflammatory changes via the release of cytokines, damage-associated molecular patterns (DAMPs), and pathogen-associated molecular patterns (PAMPs), respectively. The impact of these noxious agents on the survival and function of the enteric nervous system (ENS) is poorly understood. Here, we show that in contrast to an expected decrease, experimental as well as clinical colitis causes an increase in the transcript levels of enteric neuronal and glial genes. Immunostaining revealed an elevated neuronal innervation of the inflamed regions of the gut mucosa. The increase was seen in models with overt damage to epithelial cells and models of T cell-induced colitis. Transcriptomic data from treatment naïve pediatric IBD patients also confirmed the increase in the neuroglial genes and were replicated on an independent adult IBD dataset. This induction in the neuroglial genes was transient as levels returned to normal upon the induction of remission in both mouse models as well as colitis patients. Our data highlight the dynamic and robust nature of the enteric nervous system in colitis and open novel questions on its regulation. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Inflammatory Bowel Disease)
►▼ Show Figures

Figure 1

10 pages, 1655 KiB  
Article
Pathological Role of Pin1 in the Development of DSS-Induced Colitis
by Yasuka Matsunaga, Shun Hasei, Takeshi Yamamotoya, Hiroaki Honda, Akifumi Kushiyama, Hideyuki Sakoda, Midori Fujishiro, Hiraku Ono, Hisanaka Ito, Takayoshi Okabe, Tomoichiro Asano and Yusuke Nakatsu
Cells 2021, 10(5), 1230; https://doi.org/10.3390/cells10051230 - 17 May 2021
Cited by 7 | Viewed by 3061
Abstract
Inflammatory bowel diseases (IBDs) are serious disorders of which the etiologies are not, as yet, fully understood. In this study, Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) protein was shown to be dramatically upregulated in the colons of dextran sodium sulfate (DSS)-induced ulcerative colitis [...] Read more.
Inflammatory bowel diseases (IBDs) are serious disorders of which the etiologies are not, as yet, fully understood. In this study, Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) protein was shown to be dramatically upregulated in the colons of dextran sodium sulfate (DSS)-induced ulcerative colitis model mice. Interestingly, Pin1 knockout (KO) mice exhibited significant attenuation of DSS-induced colitis compared to wild-type (WT) mice, based on various parameters, including body weight, colon length, microscopic observation of the intestinal mucosa, inflammatory cytokine expression, and cleaved caspase-3. In addition, a role of Pin1 in inflammation was suggested because the percentage of M1-type macrophages in the colon was decreased in the Pin1 KO mice while that of M2-type macrophages was increased. Moreover, Pin1 KO mice showed downregulation of both Il17 and Il23a expression in the colon, both of which have been implicated in the development of colitis. Finally, oral administration of Pin1 inhibitor partially but significantly prevented DSS-induced colitis in mice, raising the possibility of Pin1 inhibitors serving as therapeutic agents for IBD. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Inflammatory Bowel Disease)
►▼ Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1871 KiB  
Review
Bile Acids Activated Receptors in Inflammatory Bowel Disease
by Michele Biagioli, Silvia Marchianò, Adriana Carino, Cristina Di Giorgio, Luca Santucci, Eleonora Distrutti and Stefano Fiorucci
Cells 2021, 10(6), 1281; https://doi.org/10.3390/cells10061281 - 21 May 2021
Cited by 40 | Viewed by 5868
Abstract
Once known exclusively for their role in nutrients absorption, bile acids have emerged as signaling molecules, generated from cholesterol breakdown, acting on several immune cells by activating a variety of receptors including the G protein-coupled bile acid receptor 1 (GPABR1 or TGR5), the [...] Read more.
Once known exclusively for their role in nutrients absorption, bile acids have emerged as signaling molecules, generated from cholesterol breakdown, acting on several immune cells by activating a variety of receptors including the G protein-coupled bile acid receptor 1 (GPABR1 or TGR5), the Farnesoid-X-receptor (FXR) and, as recently discovered, the retinoid-related orphan receptors (ROR)γt. GPBAR1, FXR, and RORγt are highly expressed in cells of the innate and adaptive immune system (i.e., dendritic cells (DCs), macrophages, innate lymphoid 3 cells (ILC3s), and T helper 17 (Th17) lymphocytes) and plays an important role in regulating intestinal and liver immunity, highlighting a role for various bile acid species in regulating immune responses to intestinal microbial antigens. While primary bile acids are generated from the cholesterol breakdown secondary bile acids, the GPBAR1 ligands, and oxo-bile acids derivatives, the RORγt ligands, are generated by the intestinal microbiota, highlighting the potential of these bile acids in mediating the chemical communication between the intestinal microbiota and the host. Changes in intestinal microbiota, dysbiosis, alter the composition of the bile acid pool, promoting the activation of the immune system and development of chronic inflammation. In this review, we focus on the molecular mechanisms by which an altered bile acid signaling promotes intestinal inflammation. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Inflammatory Bowel Disease)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop