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Changing Paradigms in Inflammatory Bowel Diseases
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Changing Paradigms in Inflammatory Bowel Diseases

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 October 2021) | Viewed by 14809

Special Issue Editors

Prof. Dr. Christoph Becker

E-Mail Website
Guest Editor
Medizinische Klinik 1- Gastroenterologie, Pneumologie und Endokrinologie Universitätsklinikum Erlangen, Erlangen, Germany
Interests: physiology and pathophysiology of the gut
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Britta Siegmund

E-Mail Website
Guest Editor
Medizinische Klinik für Gastroenterologie, Infektiologie und Rheumatologie CBF, Charitè Universitätsmedizin, Berlin, Germany
Interests: physiology and pathophysiology of the gut
Special Issues, Collections and Topics in MDPI journals
Dr. Eva Liebing

E-Mail Website
Co-Guest Editor
Department of Medicine 1, University Hospital, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany
Interests: intestinal organoids; physiology and pathophysiology of the gut
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Inflammatory bowel diseases (IBD), which include Crohn’s disease and ulcerative colitis, affect an estimated 10 million people worldwide. IBD is characterized by episodes of inflammatory flares and periods of remission. These chronic, life-long conditions can be treated but not cured. Since the cause of IBD is still unknown, recent interest has focused on the role of dysregulated signal exchange between the epithelium and immune cells and the resulting consequences for the course of disease. Increased expression of pro-inflammatory cytokines is a hallmark of chronic intestinal inflammation. However, cytokines such as TNFα, IL22 and IL33 have recently emerged as key players also in the regulation of epithelial cell function, giving clear evidence that inflammatory cytokines do not only activate immune cells but also directly affect epithelial cells and thereby regulate homeostasis and intestinal barrier function. While cytokines affect IEC functions and homeostasis, IEC in turn regulate bacterial translocation and respond to signals from neighboring bacteria shaping the activation and the nature of the mucosal immune response. This Special Issue will focus on recent discoveries in the field of IBD, which have changed paradigms and have the potential for novel pathophysiological concepts. We specifically aim for original articles and reviews highlighting the significance of immune-epithelial crosstalk, novel cellular and molecular players and systems biology approaches in IBD development.

Prof. Dr. Christoph Becker
Prof. Dr. Britta Siegmund
Dr. Eva Liebing
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

  • inflammatory bowel diseases
  • intestinal barrier
  • chronic inflammation
  • mucosa
  • immune cells
  • epithelial cells
  • therapy
  • homeostasis
  • cytokine signaling pathways

Published Papers (4 papers)

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Research

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19 pages, 2834 KiB  
Article
Macrophages Compensate for Loss of Protein Tyrosine Phosphatase N2 in Dendritic Cells to Protect from Elevated Colitis
by Larissa Hering, Egle Katkeviciute, Marlene Schwarzfischer, Anna Niechcial, Julianne B. Riggs, Marcin Wawrzyniak, Kirstin Atrott, Marnix van de Sande, Silvia Lang, Burkhard Becher, Gerhard Rogler, Michael Scharl and Marianne R. Spalinger
Int. J. Mol. Sci. 2021, 22(13), 6820; https://doi.org/10.3390/ijms22136820 - 25 Jun 2021
Cited by 3 | Viewed by 2428
Abstract
Protein tyrosine phosphatase nonreceptor type 2 (PTPN2) plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Mice lacking PTPN2 in dendritic cells (DCs) develop skin and liver inflammation by the age of 22 weeks due to a generalized loss of [...] Read more.
Protein tyrosine phosphatase nonreceptor type 2 (PTPN2) plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Mice lacking PTPN2 in dendritic cells (DCs) develop skin and liver inflammation by the age of 22 weeks due to a generalized loss of tolerance leading to uncontrolled immune responses. The effect of DC-specific PTPN2 loss on intestinal health, however, is unknown. The aim of this study was to investigate the DC-specific role of PTPN2 in the intestine during colitis development. PTPN2fl/flxCD11cCre mice were subjected to acute and chronic DSS colitis as well as T cell transfer colitis. Lamina propria immune cell populations were analyzed using flow cytometry. DC-specific PTPN2 deletion promoted infiltration of B and T lymphocytes, macrophages, and DCs into the lamina propria of unchallenged mice and elevated Th1 abundance during acute DSS colitis, suggesting an important role for PTPN2 in DCs in maintaining intestinal immune cell homeostasis. Surprisingly, those immune cell alterations did not translate into increased colitis susceptibility in acute and chronic DSS-induced colitis or T cell transfer colitis models. However, macrophage depletion by clodronate caused enhanced colitis severity in mice with a DC-specific loss of PTPN2. Loss of PTPN2 in DCs affects the composition of lamina propria lymphocytes, resulting in increased infiltration of innate and adaptive immune cells. However, this did not result in an elevated colitis phenotype, likely because increased infiltration of macrophages in the intestine upon loss of PTPN2 loss in DCs can compensate for the inflammatory effect of PTPN2-deficient DCs. Full article
(This article belongs to the Special Issue Changing Paradigms in Inflammatory Bowel Diseases)
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15 pages, 4056 KiB  
Article
Dynamic Imaging of IEL-IEC Co-Cultures Allows for Quantification of CD103-Dependent T Cell Migration
by Karin Enderle, Martin Dinkel, Eva-Maria Spath, Benjamin Schmid, Sebastian Zundler, Philipp Tripal, Markus F. Neurath, Kai Hildner and Clemens Neufert
Int. J. Mol. Sci. 2021, 22(10), 5148; https://doi.org/10.3390/ijms22105148 - 13 May 2021
Cited by 5 | Viewed by 2904
Abstract
Intraepithelial lymphocytes (IEL) are widely distributed within the small intestinal epithelial cell (IEC) layer and represent one of the largest T cell pools of the body. While implicated in the pathogenesis of intestinal inflammation, detailed insight especially into the cellular cross-talk between IELs [...] Read more.
Intraepithelial lymphocytes (IEL) are widely distributed within the small intestinal epithelial cell (IEC) layer and represent one of the largest T cell pools of the body. While implicated in the pathogenesis of intestinal inflammation, detailed insight especially into the cellular cross-talk between IELs and IECs is largely missing in part due to lacking methodologies to monitor this interaction. To overcome this shortcoming, we employed and validated a murine IEL-IEC (organoids) ex vivo co-culture model system. Using livecell imaging we established a protocol to visualize and quantify the spatio-temporal migratory behavior of IELs within organoids over time. Applying this methodology, we found that IELs lacking CD103 (i.e., integrin alpha E, ITGAE) surface expression usually functioning as a retention receptor for IELs through binding to E-cadherin (CD324) expressing IECs displayed aberrant mobility and migration patterns. Specifically, CD103 deficiency affected the ability of IELs to migrate and reduced their speed during crawling within organoids. In summary, we report a new technology to monitor and quantitatively assess especially migratory characteristics of IELs communicating with IEC ex vivo. This approach is hence readily applicable to study the effects of targeted therapeutic interventions on IEL-IEC cross-talk. Full article
(This article belongs to the Special Issue Changing Paradigms in Inflammatory Bowel Diseases)
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Review

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16 pages, 1093 KiB  
Review
Mucins Dynamics in Physiological and Pathological Conditions
by Hassan Melhem, Daniel Regan-Komito and Jan Hendrik Niess
Int. J. Mol. Sci. 2021, 22(24), 13642; https://doi.org/10.3390/ijms222413642 - 20 Dec 2021
Cited by 21 | Viewed by 3710
Abstract
Maintaining intestinal health requires clear segregation between epithelial cells and luminal microbes. The intestinal mucus layer, produced by goblet cells (GCs), is a key element in maintaining the functional protection of the epithelium. The importance of the gut mucus barrier is highlighted in [...] Read more.
Maintaining intestinal health requires clear segregation between epithelial cells and luminal microbes. The intestinal mucus layer, produced by goblet cells (GCs), is a key element in maintaining the functional protection of the epithelium. The importance of the gut mucus barrier is highlighted in mice lacking Muc2, the major form of secreted mucins. These mice show closer bacterial residence to epithelial cells, develop spontaneous colitis and became moribund when infected with the attaching and effacing pathogen, Citrobacter rodentium. Furthermore, numerous observations have associated GCs and mucus layer dysfunction to the pathogenesis of inflammatory bowel disease (IBD). However, the molecular mechanisms that regulate the physiology of GCs and the mucus layer remain obscured. In this review, we consider novel findings describing divergent functionality and expression profiles of GCs subtypes within intestinal crypts. We also discuss internal (host) and external (diets and bacteria) factors that modulate different aspects of the mucus layer as well as the contribution of an altered mucus barrier to the onset of IBD. Full article
(This article belongs to the Special Issue Changing Paradigms in Inflammatory Bowel Diseases)
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18 pages, 802 KiB  
Review
The Gut-Brain Axis in Inflammatory Bowel Disease—Current and Future Perspectives
by Claudia Günther, Veit Rothhammer, Marisa Karow, Markus F. Neurath and Beate Winner
Int. J. Mol. Sci. 2021, 22(16), 8870; https://doi.org/10.3390/ijms22168870 - 18 Aug 2021
Cited by 33 | Viewed by 5044
Abstract
The gut–brain axis is a bidirectional communication system driven by neural, hormonal, metabolic, immunological, and microbial signals. Signaling events from the gut can modulate brain function and recent evidence suggests that the gut–brain axis may play a pivotal role in linking gastrointestinal and [...] Read more.
The gut–brain axis is a bidirectional communication system driven by neural, hormonal, metabolic, immunological, and microbial signals. Signaling events from the gut can modulate brain function and recent evidence suggests that the gut–brain axis may play a pivotal role in linking gastrointestinal and neurological diseases. Accordingly, accumulating evidence has suggested a link between inflammatory bowel diseases (IBDs) and neurodegenerative, as well as neuroinflammatory diseases. In this context, clinical, epidemiological and experimental data have demonstrated that IBD predisposes a person to pathologies of the central nervous system (CNS). Likewise, a number of neurological disorders are associated with changes in the intestinal environment, which are indicative for disease-mediated gut–brain inter-organ communication. Although this axis was identified more than 20 years ago, the sequence of events and underlying molecular mechanisms are poorly defined. The emergence of precision medicine has uncovered the need to take into account non-intestinal symptoms in the context of IBD that could offer the opportunity to tailor therapies to individual patients. The aim of this review is to highlight recent findings supporting the clinical and biological link between the gut and brain, as well as its clinical significance for IBD as well as neurodegeneration and neuroinflammation. Finally, we focus on novel human-specific preclinical models that will help uncover disease mechanisms to better understand and modulate the function of this complex system. Full article
(This article belongs to the Special Issue Changing Paradigms in Inflammatory Bowel Diseases)
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