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Precision Medicine for Inflammatory and Autoimmune Diseases
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Precision Medicine for Inflammatory and Autoimmune Diseases

A special issue of Journal of Personalized Medicine (ISSN 2075-4426).

Deadline for manuscript submissions: closed (15 December 2021) | Viewed by 17926

Special Issue Editor

Dr. Michael Freeley

E-Mail Website
Guest Editor
School of Biotechnology, Dublin City University, Dublin, Ireland
Interests: immunology techniques; kinase; cell culture; cell migration; immunology; t lymphocytes; flow cytometry; phosphorylation; adaptive immunity; signaling pathways

Special Issue Information

Dear colleagues,

Advances in precision medicine are enabling diseases and conditions to be diagnosed more accurately through molecular analysis and treatments to be applied that target the underlying aberrant pathway or target, thus resulting in a stratified or individualised approach to therapy. While it is clear that the most significant advances in precision medicine have been made in oncology, where molecular profiling of patient tumours facilitates treatment with targeted therapies resulting in improved tumour control and increased survival, tailoring of medical treatments is now also being applied to other conditions, including inherited diseases. This is best exemplified by the exciting advances made in the treatment of cystic fibrosis, where molecular profiling of the mutation(s) within the gene encoding the Cystic Fibrosis Transmembrane Receptor enables the tailoring of small molecule drugs that target the products of the underlying mutation(s) for cohorts of patients. Hence, prevision medicine is facilitating a shift away from the One-Size-Fits-All and Trial-and-Error approach to an individualised and stratified approach. On the other hand, while there have been numerous targeted therapies that are now clinically approved for the treatment of inflammatory and autoimmune diseases, patients are still largely treated on a One-Size-Fits-All and Trial-and-Error approach, resulting in poor disease control and/or exacerbation for significant patient cohorts, patient dissatisfaction, and unnecessary healthcare costs. Therefore, there is a significant unmet clinical need to identify which patients are more likely to benefit from a therapeutic drug while at the same time identifying patients who are unlikely to benefit from the drug so that alternative treatment strategies can be pursued.

The aim of this Special Issue will be to provide a comprehensive overview of the progress, challenges, and opportunities for patient stratification and treatment of inflammatory and autoimmune diseases, with a particular focus on Rheumatoid Arthritis, Psoriasis, Psoriatic Arthritis, Multiple Sclerosis, and Inflammatory Bowel Disease.

Dr. Michael Freeley
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. Journal of Personalized Medicine is an international peer-reviewed open access monthly 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 2600 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

  • precision medicine
  • personalised medicine
  • molecular diagnostics
  • targeted therapy
  • inflammatory disease
  • autoimmune disease
  • rheumatoid arthritis
  • psoriasis
  • psoriatic arthritis
  • multiple sclerosis
  • inflammatory bowel disease

Published Papers (6 papers)

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Research

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11 pages, 692 KiB  
Article
Serum Interleukin (IL)-23 and IL-17 Profile in Inflammatory Bowel Disease (IBD) Patients Could Differentiate between Severe and Non-Severe Disease
by Laura A. Lucaciu, Maria Ilieș, Ștefan C. Vesa, Radu Seicean, Shahida Din, Cristina Adela Iuga and Andrada Seicean
J. Pers. Med. 2021, 11(11), 1130; https://doi.org/10.3390/jpm11111130 - 2 Nov 2021
Cited by 13 | Viewed by 2484
Abstract
Interleukin (IL)-17 and IL-23 are crucial for mediating gut mucosal inflammation in inflammatory bowel disease (IBD), which has led to new therapeutic strategies. We assessed the relevancy of IL-17 and IL-23 serum levels as potential biomarkers towards severe IBD discrimination and disease-related complications. [...] Read more.
Interleukin (IL)-17 and IL-23 are crucial for mediating gut mucosal inflammation in inflammatory bowel disease (IBD), which has led to new therapeutic strategies. We assessed the relevancy of IL-17 and IL-23 serum levels as potential biomarkers towards severe IBD discrimination and disease-related complications. Sixty-two patients diagnosed with Crohn’s disease (CD) and ulcerative colitis (UC) were included. Serum IL-17 and IL-23 were measured by sandwich enzyme-linked immunosorbent assays (ELISA). IL-23 and fecal calprotectin (FCal) were significantly higher in severe CD (p < 0.001) and UC (p < 0.001 and p = 0.001, respectively), compared to mild or moderate. Elevated C-reactive protein (CRP) was correlated with severe disease only in CD (p = 0.008), whereas for UC, disease severity was associated with increased IL-17 values (p < 0.001). Diagnostic role of IL-23 was superior to FCal in discriminating between severe and mild to moderate CD (p < 0.001). IL-23 levels were also significantly higher in CD patients with intestinal complications (p = 0.04). Both IL-17 and IL-23 correlate with IBD severity, and IL-23 might be a promising novel biomarker for severe CD. Identifying the dominant IL pathway involved in IBD severity could serve as guidance for clinical decision-making on biologic therapy. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)
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24 pages, 4942 KiB  
Article
Metabolomic Biomarker Candidates for Skeletal Muscle Loss in the Collagen-Induced Arthritis (CIA) Model
by Paulo V. G. Alabarse, Jordana M. S. Silva, Rafaela C. E. Santo, Marianne S. Oliveira, Andrelise S. Almeida, Mayara S. de Oliveira, Mônica L. Immig, Eduarda C. Freitas, Vivian O. N. Teixeira, Camilla L. Bathurst, Claiton V. Brenol, Lidiane I. Filippin, Stephen P. Young, Priscila S. Lora and Ricardo M. Xavier
J. Pers. Med. 2021, 11(9), 837; https://doi.org/10.3390/jpm11090837 - 26 Aug 2021
Cited by 6 | Viewed by 2928
Abstract
There is no consensus for diagnosis or treatment of RA muscle loss. We aimed to investigate metabolites in arthritic mice urine as biomarkers of muscle loss. DBA1/J mice comprised collagen-induced arthritis (CIA) and control (CO) groups. Urine samples were collected at 0, 18, [...] Read more.
There is no consensus for diagnosis or treatment of RA muscle loss. We aimed to investigate metabolites in arthritic mice urine as biomarkers of muscle loss. DBA1/J mice comprised collagen-induced arthritis (CIA) and control (CO) groups. Urine samples were collected at 0, 18, 35, 45, 55, and 65 days of disease and subjected to nuclear magnetic resonance spectroscopy. Metabolites were identified using Chenomx and Birmingham Metabolite libraries. The statistical model used principal component analysis, partial least-squares discriminant analysis, and partial least-squares regression analysis. Linear regression and Fisher’s exact test via the MetaboAnalyst website were performed (VIP-score). Nearly 100 identified metabolites had CIA vs. CO and disease time-dependent differences (p < 0.05). Twenty-eight metabolites were muscle-associated: carnosine (VIPs 2.8 × 102) and succinyl acetone (VIPs 1.0 × 10) showed high importance in CIA vs. CO models at day 65; CIA pair analysis showed histidine (VIPs 1.2 × 102) days 55 vs. 65, histamine (VIPs 1.1 × 102) days 55 vs. 65, and L-methionine (VIPs 1.1 × 102) days 0 vs. 18. Carnosine was fatigue- (0.039) related, creatine was food intake- (−0.177) and body weight- (−0.039) related, and both metabolites were clinical score- (0.093; 0.050) and paw edema- (0.125; 0.026) related. Therefore, muscle metabolic alterations were detected in arthritic mice urine, enabling further validation in RA patient’s urine, targeting prognosis, diagnosis, and monitoring of RA-mediated muscle loss. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)
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10 pages, 288 KiB  
Article
IL17F: A Possible Risk Marker for Spondyloarthritis in HLA-B*27 Negative Brazilian Patients
by Janisleya Silva Ferreira Neves, Jeane Eliete Laguila Visentainer, Denise Manjurma da Silva Reis, Marco Antonio Rocha Loures, Hugo Vicentin Alves, Joana Maira Valentini Zacarias and Ana Maria Sell
J. Pers. Med. 2021, 11(6), 520; https://doi.org/10.3390/jpm11060520 - 7 Jun 2021
Cited by 4 | Viewed by 2404
Abstract
HLA-B*27 is an important marker for spondyloarthritis (SpA), however, many SpA patients are HLA-B*27 negative. Thus, the aim of this study was to investigate the influence of IL17, TNF and VDR gene polymorphisms in SpA patients who were HLA-B*27 negative. This case-control [...] Read more.
HLA-B*27 is an important marker for spondyloarthritis (SpA), however, many SpA patients are HLA-B*27 negative. Thus, the aim of this study was to investigate the influence of IL17, TNF and VDR gene polymorphisms in SpA patients who were HLA-B*27 negative. This case-control study was conducted in 158 patients [102 patients with ankylosing spondylitis (AS) and 56 with psoriatic arthritis (PsA)] and 184 controls. HLA-B*27 genotyping was performed using PCR-SSP and IL17A (rs2275913), IL17F (rs763780), TNF-308 (rs1800629), TNF-238 (rs361525), FokI C>T (rs2228570), TaqI C>T (rs731236), ApaI A>C (rs7975232), and BsmI C>T (rs1544410) using PCR-RFLP. Statistical analyses were performed by Chi-square and logistic regression using OpenEpi and SNPStats software. The IL17F C allele frequency was higher in patients with SpA, AS and PsA compared to controls. The IL17F T/C genotype frequency was higher in SpA patients in an overdominant inheritance model and when men and women were separately analyzed. IL17A_IL17F AC haplotype was significantly associated to the risk for SpA patients. As for VDR, the ApaI a/a was a potential risk factor for SpA in men. In conclusion, IL17F C variant contributed to the risk of SpA in Brazilian patients who were HLA-B*27 negative and could be a potential marker for SpA. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)
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9 pages, 257 KiB  
Article
Prognostic Factors for Radiographic Progression in Patients with Seronegative Rheumatoid Arthritis
by Eun-Jung Park, WooSeong Jeong and Jinseok Kim
J. Pers. Med. 2021, 11(3), 184; https://doi.org/10.3390/jpm11030184 - 5 Mar 2021
Cited by 5 | Viewed by 1744
Abstract
(1) Background: It has long been suggested that seronegative rheumatoid arthritis (RA) represents a clinical entity quite distinct from that of seropositive. However, analytical studies of seronegative RA dedicated to clinical outcomes regarding radiographic progression and related risk factors are scarce. The aim [...] Read more.
(1) Background: It has long been suggested that seronegative rheumatoid arthritis (RA) represents a clinical entity quite distinct from that of seropositive. However, analytical studies of seronegative RA dedicated to clinical outcomes regarding radiographic progression and related risk factors are scarce. The aim of this study is to evaluate radiographic outcome and prognostic factors for radiographic progression in patients with seronegative rheumatoid arthritis. (2) Methods: Subjects included RA patients reported as seronegative for both rheumatoid factor and anti-citrullinated protein antibody, who were treated at Jeju National University Hospital in South Korea between 2003 and 2016, including follow-up of at least 2 years. All patients fulfilled 1987 ACA or 2010 ACR/EULAR RA criteria. Radiographic progression was measured by yearly change in the Sharp van der Heijde (SvdH) score during follow-up periods. Medical records, laboratory and radiographic data were retrospectively analyzed, and linear regression analysis was performed to evaluate prognostic factors for radiographic progression in patients with seronegative rheumatoid arthritis. (3) Results: In total, 116 patients with seronegative RA were observed and 43 (37.1%) patients demonstrated radiographic damage during follow-up period. Mean age at diagnosis was 48 years and 86 (74.1%) patients were female. Symptom duration at diagnosis was 1.3 years and mean follow-up duration was 5.2 years. Patients with radiographic damage at diagnosis were 14 (12.1%) and mean SvdH score was 6.8 at diagnosis. Radiographic damage and SvdH at diagnosis significantly correlated with radiographic progression in patients with seronegative RA after adjusting age, sex, symptom duration, number of active synovitis, and CRP at diagnosis (β-coefficient 6.5 ± 1.84; p = 0.001 and β-coefficient 0.12 ± 0.02; p < 0.001, respectively). (4) Conclusions: This study determined that radiographic damage and SvdH at diagnosis were predictive factors in progression of radiographic damage in patients with seronegative rheumatoid arthritis. A large comparative study dedicated to this issue in seronegative RA is required. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)

Review

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14 pages, 535 KiB  
Review
Advances of Genomic Medicine in Psoriatic Arthritis
by Carlos M. Laborde, Leyre Larzabal, Álvaro González-Cantero, Patricia Castro-Santos and Roberto Díaz-Peña
J. Pers. Med. 2022, 12(1), 35; https://doi.org/10.3390/jpm12010035 - 3 Jan 2022
Cited by 3 | Viewed by 2432
Abstract
Psoriatic arthritis (PsA) is a common type of inflammatory arthritis found in up to 40% of patients with psoriasis. Although early diagnosis is important for reducing the risk of irreversible structural damage, there are no adequate screening tools for this purpose, and there [...] Read more.
Psoriatic arthritis (PsA) is a common type of inflammatory arthritis found in up to 40% of patients with psoriasis. Although early diagnosis is important for reducing the risk of irreversible structural damage, there are no adequate screening tools for this purpose, and there are no clear markers of predisposition to the disease. Much evidence indicates that PsA disorder is complex and heterogeneous, where genetic and environmental factors converge to trigger inflammatory events and the development of the disease. Nevertheless, the etiologic events that underlie PsA are complex and not completely understood. In this review, we describe the existing data in PsA in order to highlight the need for further research in this disease to progress in the knowledge of its pathobiology and to obtain early diagnosis tools for these patients. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)
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12 pages, 1417 KiB  
Review
Is Metformin a Possible Beneficial Treatment for Psoriasis? A Scoping Review
by Ana Maria Alexandra Stanescu, Anca Angela Simionescu, Mira Florea and Camelia Cristina Diaconu
J. Pers. Med. 2021, 11(4), 251; https://doi.org/10.3390/jpm11040251 - 30 Mar 2021
Cited by 7 | Viewed by 4661
Abstract
Psoriasis is a chronic inflammatory condition with genetic, immunological, and metabolic etiology. The link between psoriasis and diabetes mellitus has been shown in genetic predisposition, environmental influences, inflammatory pathways, and insulin resistance, resulting in end-organ damage in both conditions. Because comorbidities often accompany [...] Read more.
Psoriasis is a chronic inflammatory condition with genetic, immunological, and metabolic etiology. The link between psoriasis and diabetes mellitus has been shown in genetic predisposition, environmental influences, inflammatory pathways, and insulin resistance, resulting in end-organ damage in both conditions. Because comorbidities often accompany psoriasis, the therapeutic management of the disease must also take into consideration the comorbidities. Given that metformin’s therapeutic role in psoriasis is not yet fully elucidated, we raised the question of whether metformin is a viable alternative for the treatment of psoriasis. We conducted this scoping review by searching for evidence in PubMed, Cochrane, and Scopus databases, and we used an extension for scoping reviews (PRISMA-ScR). Current evidence suggests that metformin is safe to use in psoriasis. Studies have shown an excellent therapeutic response to metformin in patients with psoriasis and comorbidities such as diabetes, metabolic syndrome, and obesity. There is no clear evidence supporting metformin monotherapy in patients with psoriasis without comorbidities. There is a need to further evaluate metformin in larger clinical trials, as a therapy in psoriasis. Full article
(This article belongs to the Special Issue Precision Medicine for Inflammatory and Autoimmune Diseases)
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