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Autoimmune Arthritis and Inflammatory Bowel Diseases

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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 2021) | Viewed by 12568

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Special Issue Editor

Dr. Bruno Laganà

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Guest Editor

Department of Clinical and Molecular Medicine, Sant’Andrea UniversityHospital, Sapienza University of Rome, 00185 Rome, Italy
Interests: autoimmunity; microbiota; diagnosis and treatment of rheumatoid arthritis and spondyloarthritis

Special Issue Information

Dear Colleagues,

Autoimmune arthritis, such as rheumatoid arthritis and spondyloarthritis, share different genetic, immunologic, and clinical features with Inflammatory Bowel Diseases (IBD). The coexistence of both conditions, known as enteropathic SpA, represents evidence for the gut-joint axis. The translocation of intestinal microbes caused by the increased permeability of the intestinal epithelial cell layer, or increased exposure to microbial products play a central role in connecting gut dysbiosis and joint inflammation. Several abnormalities in the gut microbiota have been reported both in patients with IBD and autoimmune arthritis, and a deeper understanding of the microbiota composition and function seems to be promising for the identification of diagnostic and predictive biomarkers.

We invite researchers to submit original molecular research and review articles in the pathogenesis of autoimmune arthritis and inflammatory bowel diseases. Potential topics include but are not limited to the following:

The evaluation of the immunological milieu and biomarkers which could help to monitor disease severity and therapeutic outcome in patients with autoimmune arthritis and inflammatory bowel diseases;
The analysis of the gut/oral/lung microbiota in autoimmune arthritis and inflammatory bowel disease patients;
Multidisciplinary approach to the diagnostic and therapeutic handling of patients affected by entheropaticspondyloarthritis.

Dr. Bruno Laganà
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. 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

autoimmune arthritis
inflammatory bowel diseases
microbiota composition
biomarkers
molecular mechanisms

Published Papers (4 papers)

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Research

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17 pages, 3274 KiB

Open AccessArticle

Modulation of PTPN2/22 Function by Spermidine in CRISPR-Cas9-Edited T-Cells Associated with Crohn’s Disease and Rheumatoid Arthritis

by Ameera M. Shaw, Ahmad Qasem and Saleh A. Naser

Int. J. Mol. Sci. 2021, 22(16), 8883; https://doi.org/10.3390/ijms22168883 - 18 Aug 2021

Cited by 6 | Viewed by 2820

Abstract

Crohn’s Disease (CD) and Rheumatoid Arthritis (RA) share some single nucleotide polymorphisms (SNPs) in protein tyrosine phosphatase non-receptor types 2 and 22 (PTPN2/22). Recently, we reported that clinical samples from CD and RA patients associated with PTPN2:rs478582 or PTPN22:rs2476601 genotypes were linked to overactive immune response and exacerbation of inflammation. Here, we investigated in vitro the effects of these SNPs in Jurkat T-cells using CRISPR-Cas9. All cells were evaluated for PTPN22/22 loss of function and effects on cell response. We measured gene expression via RT-qPCR and cytokines by ELISA. We also measured cell proliferation using a BrdU labeling proliferation ELISA, and T-cell activation using CD-25 fluorescent immunostaining. In PTPN2 SNP-edited cells, PTPN2 expression decreased by 3.2-fold, and proliferation increased by 10.2-fold compared to control. Likewise, expression of PTPN22 decreased by 2.4-fold and proliferation increased by 8.4-fold in PTPN22 SNP-edited cells. IFN-γ and TNF-α secretions increased in both edited cell lines. CD25 expression (cell activation) was 80.32% in PTPN2 SNP-edited cells and 85.82% in PTPN22 SNP-edited cells compared to 70.48% in unedited Jurkat T-cells. Treatment of PTPN2 and PTPN22-edited cells with a maximum 20 μM spermidine restored PTPN2/22 expression and cell response including cell proliferation, activation, and cytokines secretion. Most importantly, the effect of spermidine on edited cells restored normal expression and secretion of IFN-γ and TNF-α. The data clearly demonstrated that edited SNPs in PTPN2 or PTPN22 were associated with reduced gene expression, which resulted in an increase in cell proliferation and activation and overactive immune response. The data validated our earlier observations in CD and RA clinical samples. Surprisingly, spermidine restored PTPN2/22 expression in edited Jurkat T-cells and the consequent beneficial effect on cell response and inflammation. The study supports the use of polyamines dietary supplements for management of CD and in RA patients. Full article

(This article belongs to the Special Issue Autoimmune Arthritis and Inflammatory Bowel Diseases)

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Review

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18 pages, 794 KiB

Open AccessReview

Tumor Necrosis Factor’s Pathway in Crohn’s Disease: Potential for Intervention

by Cristiano Pagnini and Fabio Cominelli

Int. J. Mol. Sci. 2021, 22(19), 10273; https://doi.org/10.3390/ijms221910273 - 24 Sep 2021

Cited by 8 | Viewed by 3190

Abstract

Crohn’s disease (CD) is a chronic disorder characterized by full thickness patchy inflammation of the gastrointestinal tract. The pathogenesis is multifactorial and involves defective innate immune responses, microbiome alterations, and dysregulated activation of the acquired component of mucosal immunity. One of the molecular mediators that is involved at different levels in the initiation and progression of intestinal inflammation characteristic of CD is tumor necrosis factor (TNF). The present manuscript provides a comprehensive review focused on the potential role of TNF in the different phases of CD pathogenesis, particularly in light of its potential clinical implications. Currently available drugs blocking TNF are evaluated and discussed, specifically for open issues that still remain utilizing such therapy. TNF exerts a paramount role in the established phase of intestinal inflammation that characterizes CD patients, and anti-TNF biologics have definitely changed patient management, offering effective and safe options of treatment. Nonetheless, many patients still do not respond to anti-TNF therapy or experience unwanted side-effects. This could partially be due to the role that TNF plays in intestinal homeostasis that is particularly important during the early phase of the inflammatory process. In fact, emerging evidence supporting the dichotomous role of TNF and the identification of molecular markers will guide a more tailored and refined therapy for CD patients in the near future. Full article

(This article belongs to the Special Issue Autoimmune Arthritis and Inflammatory Bowel Diseases)

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14 pages, 605 KiB

Open AccessReview

Inhibition of Phosphodiesterase-4 in Psoriatic Arthritis and Inflammatory Bowel Diseases

by Andrea Picchianti-Diamanti, Francesca Romana Spinelli, Maria Manuela Rosado, Fabrizio Conti and Bruno Laganà

Int. J. Mol. Sci. 2021, 22(5), 2638; https://doi.org/10.3390/ijms22052638 - 5 Mar 2021

Cited by 11 | Viewed by 3080

Abstract

Phosphodiesterases (PDEs) are a heterogeneous superfamily of enzymes which catalyze the degradation of the intracellular second messengers cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Among PDEs, PDE4 is the most widely studied and characterized isoenzyme. PDE4 blocking can lead to increased levels of intracellular cAMP, which results in down-regulation of inflammatory responses by reducing the expression of tumor necrosis factor (TNF), interleukin (IL)-23, IL-17, interferon-γ, while increasing regulatory cytokines, such as IL-10. Therefore, PDE4 has been explored as a therapeutic target for the treatment of different chronic inflammatory conditions such as psoriatic arthritis (PsA) and inflammatory bowel disease (IBD). PsA shares clinical, genetic, and pathogenic features with IBD such as ulcerative colitis (UC) and Crohn’s disease (CD), and enteropathic spondyloarthritis (eSpA) represent a frequent clinical evidence of the overlap between gut and joint diseases. Current therapeutic options in PsA patients and underlying UC are limited to synthetic immunosuppressants and anti-TNF. Apremilast is an oral PDE4 inhibitor approved for the treatment of active PsA patients with inadequate response to synthetic immunosuppressants. The efficacy and a good safety profile observed in randomized clinical trials with apremilast in PsA patients have been confirmed by few studies in a real-life scenario. In addition, apremilast led to significant improvement in clinical and endoscopic features in UC patients in a phase II RCT. By now there are no available data regarding its role in eSpA patients. In view of the above, the use of apremilast in eSpA patients is a route that deserves to be deepened. Full article

(This article belongs to the Special Issue Autoimmune Arthritis and Inflammatory Bowel Diseases)

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16 pages, 1109 KiB

Open AccessReview

Vitamin D Signaling in Gastro-Rheumatology: From Immuno-Modulation to Potential Clinical Applications

by Cristiano Pagnini, Andrea Picchianti-Diamanti, Vincenzo Bruzzese, Roberto Lorenzetti, Michele Maria Luchetti, Louis Severino Martin Martin, Roberta Pica, Palma Scolieri, Maria Lia Scribano, Costantino Zampaletta, Maria Sole Chimenti and Bruno Lagana

Int. J. Mol. Sci. 2021, 22(5), 2456; https://doi.org/10.3390/ijms22052456 - 28 Feb 2021

Cited by 4 | Viewed by 2751

Abstract

In the last decades, the comprehension of the pathophysiology of bone metabolism and its interconnections with multiple homeostatic processes has been consistently expanded. The branch of osteoimmunology specifically investigating the link between bone and immune system has been developed. Among molecular mediators potentially relevant in this field, vitamin D has been recently pointed out, and abnormalities of the vitamin D axis have been described in both in vitro and in vivo models of inflammatory bowel diseases (IBD) and arthritis. Furthermore, vitamin D deficiency has been reported in patients affected by IBD and chronic inflammatory arthritis, thus suggesting the intriguing possibility of impacting the disease activity by the administration vitamin D supplements. In the present review, the complex interwoven link between vitamin D signaling, gut barrier integrity, microbiota composition, and the immune system was examined. Potential clinical application exploiting vitamin D pathway in the context of IBD and arthritis is presented and critically discussed. A more detailed comprehension of the vitamin D effects and interactions at molecular level would allow one to achieve a novel therapeutic approach in gastro-rheumatologic inflammatory diseases through the design of specific trials and the optimization of treatment protocols. Full article

(This article belongs to the Special Issue Autoimmune Arthritis and Inflammatory Bowel Diseases)

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