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Biomedicines
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Immune Mediated Inflammatory Diseases: From an Update on Molecular and...
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Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 24260

Special Issue Editor

Dr. Frédérique Ponchel

E-Mail Website
Guest Editor
NIHR Leeds Musculoskeletal Biomedical Research Unit, University of Leeds, Leeds, UK
Interests: arthritis; T-cells; Treg; Th17; inflammation; IL6; IL7; epigenetics

Special Issue Information

Dear Colleagues,

IMIDs are common conditions which cause pain, distress and loss of function, characterised by a burden of inflammatory leading to organ damage and increased morbidity and/or mortality. Inflammation may result from or be caused by an inadequate immune response for which an autoantigen has been identified in some conditions. An underlying manifestation of this shared immune dysregulation in clinically unrelated conditions is the inappropriate activation of inflammatory cytokines, notably, IL6 or TNF-alpha.

Although treatment of IMIDs has been revolutionised by the use of targeted biologic therapies with good efficacy, speed of onset and tolerability (such as cytokines blockade initially), response to therapies remains heterogeneous between patients, while the development of resistance to treatments over time is also a reason for inadequate response. This, nonetheless, has led to a shift in the management of these conditions from an organ‐based symptom relief approach to a disease mechanism modification-based treatment. As a result, tailored approaches are now possible and recognised as a high research priority in order to give the right drug to the right patient at the right time.

The Special Issue “Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine” is related to new insight into the mechanism of in IMIDs from molecular and cellular events leading to the establishment of chronicity in these diseases, from epigenetics, gene expression, phenotyping or functional work, cytokine/chemokines networking ….etc. Research into biomarker for diagnostic, prognostic and prediction of response to treatment / relapse, are also invited from any stage of development from discovery to validation/replication studies. Both original research and comprehensive review are welcomed.

Prof. Frédérique Ponchel
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. Biomedicines 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

  • IMIDs
  • molecular pathways
  • cellular immune mechanisms
  • inflammation
  • cyokine/chemokine networks
  • biomarker
  • diagnostic, prognostic
  • response to therapy

Published Papers (6 papers)

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Research

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14 pages, 5805 KiB  
Article
Serum-Derived Neuronal Exosomal microRNAs as Stress-Related Biomarkers in an Atopic Dermatitis Model
by Minkyoung Sung, Soo-Eun Sung, Kyung-Ku Kang, Joo-Hee Choi, Sijoon Lee, KilSoo Kim, Ju-Hyeon Lim, Gun Woo Lee, Hyo-Deog Rim, Seunghee Won, Byung-Soo Kim, Kyungmin Kim, Seoyoung Jang, Sang Gyu Kwak, Jungmin Woo and Min-Soo Seo
Biomedicines 2021, 9(12), 1764; https://doi.org/10.3390/biomedicines9121764 - 25 Nov 2021
Cited by 2 | Viewed by 2302
Abstract
Chronic allergic inflammatory skin disease—atopic dermatitis (AD)—is characterized by eczema, pruritus, xeroderma, and lichenification. Psychological stress is one cause of this disease; however, psychological stress will also result from the presence of AD symptoms. Previous studies have shown that psychological stress triggers neuroinflammation [...] Read more.
Chronic allergic inflammatory skin disease—atopic dermatitis (AD)—is characterized by eczema, pruritus, xeroderma, and lichenification. Psychological stress is one cause of this disease; however, psychological stress will also result from the presence of AD symptoms. Previous studies have shown that psychological stress triggers neuroinflammation in the brain, where microRNAs (miRNAs) in the neuronal exosomes (nEVs) were analyzed to identify the composition of the miRNAs in the nEVs and how they were altered by AD. In this study, the AD model was induced by treatment with 2,4-dinitrochlorobenzene (DNCB). The expression patterns of neuroinflammation markers, such as brain-derived neurotrophic factor, cyclooxygenase-2, and glial fibrillary acidic protein, were subsequently evaluated over time. Among these groups, there was a significant difference in DNCB 14 days expression compared with the control; therefore, nEVs were isolated from serum and next-generation sequencing was performed. The results demonstrate that 9 miRNAs were upregulated and 16 were downregulated in the DNCB 14 days compared with the control. Previous studies have shown that some of these miRNAs are associated with stress and stress-induced depression, which suggests that the miRNAs in nEVs may also be stress-related biomarkers. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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16 pages, 2314 KiB  
Article
MicroRNA Expression in Extracellular Vesicles from Nasal Lavage Fluid in Chronic Rhinosinusitis
by Seungbin Cha, Eun-Hye Seo, Seung Hyun Lee, Kyung Soo Kim, Chung-Sik Oh, Jong-Seok Moon and Jin Kook Kim
Biomedicines 2021, 9(5), 471; https://doi.org/10.3390/biomedicines9050471 - 26 Apr 2021
Cited by 13 | Viewed by 2514
Abstract
Extracellular vesicles (EVs) are nanovesicles of endocytic origin released by cells and found in human bodily fluids. EVs contain both mRNA and microRNA (miRNA), which can be shuttled between cells, indicating their role in cell communication. This study investigated whether nasal secretions contain [...] Read more.
Extracellular vesicles (EVs) are nanovesicles of endocytic origin released by cells and found in human bodily fluids. EVs contain both mRNA and microRNA (miRNA), which can be shuttled between cells, indicating their role in cell communication. This study investigated whether nasal secretions contain EVs and whether these EVs contain RNA. EVs were isolated from nasal lavage fluid (NLF) using sequential centrifugation. EVs were characterized and EV sizes were identified by transmission electron microscopy (TEM). In addition, EV miRNA expression was different in the chronic rhinosinusitis without nasal polyp (CRSsNP) and chronic rhinosinusitis with nasal polyp (CRSwNP) groups. The Kyoto encyclopedia gene and genome database (KEGG) database was used to identify pathways associated with changed miRNAs in each analysis group. Twelve miRNAs were differentially expressed in NLF-EVs of CRS patients versus HCs. In addition, eight miRNAs were differentially expressed in NLF-EVs of CRSwNP versus CRSsNP patients. The mucin-type O-glycan biosynthesis was a high-ranked predicted pathway in CRS patients versus healthy controls (HCs), and the Transforming growth factor beta (TGF-β) signaling pathway was a high-ranked predicted pathway in CRSwNP versus CRSsNP patients. We demonstrated the presence of and differences in NLF-EV miRNAs between CRS patients and HCs. These findings open up a broad and novel area of research on CRS pathophysiology as driven by miRNA cell communication. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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21 pages, 4414 KiB  
Article
Neutrophil Extracellular Traps Impair Intestinal Barrier Function during Experimental Colitis
by Elliot Yi-Hsin Lin, Hsuan-Ju Lai, Yuan-Kai Cheng, Kai-Quan Leong, Li-Chieh Cheng, Yi-Chun Chou, Yu-Chun Peng, Yi-Hsuan Hsu and Hao-Sen Chiang
Biomedicines 2020, 8(8), 275; https://doi.org/10.3390/biomedicines8080275 - 05 Aug 2020
Cited by 46 | Viewed by 5782
Abstract
Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the [...] Read more.
Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the breakdown in intestinal barrier function for the pathogenesis of intestinal inflammation in mouse models of colitis. NETs were abundant in the colon of mice with colitis experimentally induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Analysis of the intestinal barrier integrity revealed that NETs impaired gut permeability, enabling the initiation of luminal bacterial translocation and inflammation. Furthermore, NETs induced the apoptosis of epithelial cells and disrupted the integrity of tight junctions and adherens junctions. Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria and attenuated intestinal inflammation in both DSS and TNBS models. We conclude that NETs serve a detrimental factor in the gut epithelial barrier function leading to the pathogenesis of mucosal inflammation during acute colitis. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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19 pages, 3221 KiB  
Article
Increased IL-2 and Reduced TGF-β Upon T-Cell Stimulation are Associated with GM-CSF Upregulation in Multiple Immune Cell Types in Multiple Sclerosis
by Jehan Aram, Nanci Frakich, Elena Morandi, Mohammed Alrouji, Amal Samaraweera, David Onion, Ian Spendlove, Sergio L. Colombo, Radu Tanasescu, Bruno Gran and Cris S. Constantinescu
Biomedicines 2020, 8(7), 226; https://doi.org/10.3390/biomedicines8070226 - 18 Jul 2020
Cited by 7 | Viewed by 4206
Abstract
Granulocyte macrophage colony stimulating factor (GM-CSF) is a pro-inflammatory cytokine produced by immune cells. Recent evidence suggests that GM-CSF plays an important role in multiple sclerosis (MS) pathogenesis. We investigated the expression and regulation of GM-CSF in different immune cells in MS. We [...] Read more.
Granulocyte macrophage colony stimulating factor (GM-CSF) is a pro-inflammatory cytokine produced by immune cells. Recent evidence suggests that GM-CSF plays an important role in multiple sclerosis (MS) pathogenesis. We investigated the expression and regulation of GM-CSF in different immune cells in MS. We also investigated the differentiation and frequency of GM-CSF-producing Th cells that do not co-express interferon (IFN)-γ or interleukin-17 (IL-17) (Th-GM cells) in MS. We found a significant increase in the percentage of GM-CSF-expressing Th cells, Th1 cells, Th-GM cells, cytotoxic T (Tc) cells, monocytes, natural killer (NK) cells, and B cells in PBMC from MS patients stimulated with T cell stimuli. Stimulated PBMC culture supernatants from MS patients contained significantly higher levels of IL-2, IL-12, IL-1β, and GM-CSF and significantly lower levels of transforming growth factor (TGF-)β. Blocking IL-2 reduced the frequency of Th-GM cells in PBMC from MS patients. The frequency of Th-GM cells differentiated in vitro from naïve CD4+ T cells was significantly higher in MS patients and was further increased in MS with IL-2 stimulation. These findings suggest that all main immune cell subsets produce more GM-CSF in MS after in vitro stimulation, which is associated with defective TGF-β and increased IL-2 and IL-12 production. Th-GM cells are increased in MS. GM-CSF may be a potential therapeutic target in MS. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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13 pages, 1282 KiB  
Article
Identification of Novel Native Autoantigens in Rheumatoid Arthritis
by Thomas B. G. Poulsen, Dres Damgaard, Malene Møller Jørgensen, Ladislav Senolt, Jonathan M. Blackburn, Claus H. Nielsen and Allan Stensballe
Biomedicines 2020, 8(6), 141; https://doi.org/10.3390/biomedicines8060141 - 29 May 2020
Cited by 16 | Viewed by 3790
Abstract
The majority of patients diagnosed with rheumatoid arthritis (RA) have developed autoantibodies against neoepitopes in proteins that have undergone post-translational modification, e.g., citrullination or carbamylation. There is growing evidence of their molecular relevance and their potential utility to improve diagnosis, patient stratification, and [...] Read more.
The majority of patients diagnosed with rheumatoid arthritis (RA) have developed autoantibodies against neoepitopes in proteins that have undergone post-translational modification, e.g., citrullination or carbamylation. There is growing evidence of their molecular relevance and their potential utility to improve diagnosis, patient stratification, and prognosis for precision medicine. Autoantibodies reacting to native proteins may also have a role in RA pathogenesis, however, their reactivity patterns remain much less studied. We hypothesized that a high-density protein array technology could shed light onto the normal and disease-related autoantibodies produced in healthy and RA patient subgroups. In an exploratory study, we investigated the global reactivity of autoantibodies in plasma pools from 15 anti-cyclic citrullinated peptide (CCP)-positive and 10 anti-CCP-negative RA patients and 10 healthy donors against more than 1600 native and unmodified human proteins using a high-density protein array. A total of 102 proteins recognized by IgG autoantibodies were identified, hereof 86 were recognized by antibodies from CCP-positive RA patients and 76 from anti-CCP-negative RA patients, but not by antibodies from healthy donors. Twenty-four of the identified autoantigens have previously been identified in synovial fluid. Multiple human proteins in their native conformation are recognized by autoantibodies from anti-CCP-positive as well as anti-CCP-negative RA patients. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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Review

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44 pages, 9484 KiB  
Review
Aptamers for Proteins Associated with Rheumatic Diseases: Progress, Challenges, and Prospects of Diagnostic and Therapeutic Applications
by Elizaveta A. Shatunova, Maksim A. Korolev, Vitaly O. Omelchenko, Yuliya D. Kurochkina, Anna S. Davydova, Alya G. Venyaminova and Mariya A. Vorobyeva
Biomedicines 2020, 8(11), 527; https://doi.org/10.3390/biomedicines8110527 - 22 Nov 2020
Cited by 10 | Viewed by 4717
Abstract
Nucleic acid aptamers capable of affine and specific binding to their molecular targets have now established themselves as a very promising alternative to monoclonal antibodies for diagnostic and therapeutic applications. Although the main focus in aptamers’ research and development for biomedicine is made [...] Read more.
Nucleic acid aptamers capable of affine and specific binding to their molecular targets have now established themselves as a very promising alternative to monoclonal antibodies for diagnostic and therapeutic applications. Although the main focus in aptamers’ research and development for biomedicine is made on cardiovascular, infectious, and malignant diseases, the use of aptamers as therapeutic or diagnostic tools in the context of rheumatic diseases is no less important. In this review, we consider the main features of aptamers that make them valuable molecular tools for rheumatologists, and summarize the studies on the selection and application of aptamers for protein biomarkers associated with rheumatic diseases. We discuss the progress in the development of aptamer-based diagnostic assays and targeted therapeutics for rheumatic disorders, future prospects in the field, and issues that have yet to be addressed. Full article
(This article belongs to the Special Issue Immune Mediated Inflammatory Diseases: From an Update on Molecular and Cellular Mechanisms to Biomarkers for Personalized Medicine)
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