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Biomolecules
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Pathogenesis of Arthritis
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Pathogenesis of Arthritis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 November 2020) | Viewed by 55750

Special Issue Editor

Prof. Dr. Alessandra Bitto

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
Interests: tissue remodeling; inflammatory pathways; angiogenesis; drug’s mechanism of action; nutraceuticals

Special Issue Information

Dear Colleagues,

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that arises more frequently in females than males, with a peak in the adult life. Presently, there are two major clinical subtypes of RA according to the presence or absence of anticitrullinated protein antibodies, with those which are negative showing less effective treatment response to methotrexate or rituximab. As for the pathogenesis of the disease, many factors have been indicated so far, specifically, susceptibility genes, epigenetic modifications, environmental, and dietetic factors. However, although all these can lead to the onset of self-protein citrullination resulting in the production of autoantibodies, none can be considered as the sole cause of arthritis.

At tissue level in the synovia, a strong leukocyte infiltrate is responsible for producing inflammatory mediators that further promote inflammation. In addition, these mediators promote interactions of fibroblast-like synoviocytes with the cells of the innate immune system, including monocytes, macrophages, mast cells, dendritic cells, and so on, as well as cells of adaptive immune system, such as T cells and B cells. Interleukins, TNF, matrix metalloproteinase, TGF, PDGF, interferons, VEGF, FGF, and many others are involved and contribute to the extent of the damage. The dramatic increase in inflammatory markers leads to synovial hyperplasia, cartilage damage, and bone erosion where the synovial membrane inserts into the periosteum. The destruction of the subchondral bone can eventually result in the degeneration of the articular cartilage as the result of a decrease in osteoblasts and an increase in osteoclasts and synoviocytes. It is therefore crucial that researchers continue to study the pathogenesis of arthritis and identify new or adjuvant treatments. This Special Issue welcomes original research and review articles covering significant developments in the pathogenesis of arthritis, or novel therapeutic approaches.

Prof. Dr. Alessandra Bitto
Guest Editor

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Keywords

  • arthritis
  • autoimmune
  • cytokines
  • inflammation

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Published Papers (11 papers)

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Research

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11 pages, 2115 KiB  
Article
Beneficial Effect of Tempol, a Membrane-Permeable Radical Scavenger, on Inflammation and Osteoarthritis in In Vitro Models
by Giovanna Calabrese, Alessio Ardizzone, Michela Campolo, Sabrina Conoci, Emanuela Esposito and Irene Paterniti
Biomolecules 2021, 11(3), 352; https://doi.org/10.3390/biom11030352 - 25 Feb 2021
Cited by 20 | Viewed by 3288
Abstract
Osteoarthritis (OA) is one of the most common and widespread diseases which is highly disabling for humans. This makes OA a chronic disease for which it is urgent to find new therapeutic strategies. The inflammatory state in OA contributes to its progression through [...] Read more.
Osteoarthritis (OA) is one of the most common and widespread diseases which is highly disabling for humans. This makes OA a chronic disease for which it is urgent to find new therapeutic strategies. The inflammatory state in OA contributes to its progression through multiple mechanisms involving the recruitment of phagocytes and leukocytes, inflammatory response, and reactive oxygen species (ROS) production. Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl) is classifiable as a piperidine nitroxide, with excellent antioxidant effects, while its anti-inflammatory role is not yet clear. On this basis, we explored its promising biological properties in two in vitro model:, macrophage (J774) and chondrocyte (CC) cell lines. With this aim in mind, we induced inflammation in J774 and CC using lipopolysaccharide (LPS) and Interleukin1β (IL-1β), and after 24, 72 and 168 h of tempol treatment analyzed their effects on cytotoxicity and anti-inflammatory activity. Our data suggested that tempol treatment is able to reduce inflammation and nitrite production in LPS-induced J774 as well as reducing the production of proinflammatory mediators including cytokines, enzymes, and metalloproteases (MMPs) in IL-1β-stimulated CC. Thus, since inflammation and oxidative stress have a crucial role in the pathogenesis and progression of OA, tempol could be considered as a new therapeutic approach for this pathology. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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11 pages, 1231 KiB  
Article
Identification and Validation of Carbonic Anhydrase II as the First Target of the Anti-Inflammatory Drug Actarit
by Ghita Ghislat, Taufiq Rahman and Pedro J. Ballester
Biomolecules 2020, 10(11), 1570; https://doi.org/10.3390/biom10111570 - 19 Nov 2020
Cited by 6 | Viewed by 3100
Abstract
Background and purpose: Identifying the macromolecular targets of drug molecules is a fundamental aspect of drug discovery and pharmacology. Several drugs remain without known targets (orphan) despite large-scale in silico and in vitro target prediction efforts. Ligand-centric chemical-similarity-based methods for in silico target [...] Read more.
Background and purpose: Identifying the macromolecular targets of drug molecules is a fundamental aspect of drug discovery and pharmacology. Several drugs remain without known targets (orphan) despite large-scale in silico and in vitro target prediction efforts. Ligand-centric chemical-similarity-based methods for in silico target prediction have been found to be particularly powerful, but the question remains of whether they are able to discover targets for target-orphan drugs. Experimental Approach: We used one of these in silico methods to carry out a target prediction analysis for two orphan drugs: actarit and malotilate. The top target predicted for each drug was carbonic anhydrase II (CAII). Each drug was therefore quantitatively evaluated for CAII inhibition to validate these two prospective predictions. Key Results: Actarit showed in vitro concentration-dependent inhibition of CAII activity with submicromolar potency (IC50 = 422 nM) whilst no consistent inhibition was observed for malotilate. Among the other 25 targets predicted for actarit, RORγ (RAR-related orphan receptor-gamma) is promising in that it is strongly related to actarit’s indication, rheumatoid arthritis (RA). Conclusion and Implications: This study is a proof-of-concept of the utility of MolTarPred for the fast and cost-effective identification of targets of orphan drugs. Furthermore, the mechanism of action of actarit as an anti-RA agent can now be re-examined from a CAII-inhibitor perspective, given existing relationships between this target and RA. Moreover, the confirmed CAII-actarit association supports investigating the repositioning of actarit on other CAII-linked indications (e.g., hypertension, epilepsy, migraine, anemia and bone, eye and cardiac disorders). Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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11 pages, 1347 KiB  
Article
Rheumatoid Arthritis: Applicability of Ready-to-Use Human Cartilaginous Cells for Screening of Compounds with TNF-Alpha Inhibitory Activity
by Larissa T. Volova, Evgeniy I. Pugachev, Victoria V. Rossinskaya, Violetta V. Boltovskaya, Dmitry A. Dolgushkin and Natalya Ossina
Biomolecules 2020, 10(11), 1563; https://doi.org/10.3390/biom10111563 - 17 Nov 2020
Cited by 2 | Viewed by 2469
Abstract
In the context of modern drug discovery, there is an obvious advantage to designing phenotypic bioassays based on human disease-relevant cells that express disease-relevant markers. The specific aim of the study was to develop a convenient and reliable method for screening compounds with [...] Read more.
In the context of modern drug discovery, there is an obvious advantage to designing phenotypic bioassays based on human disease-relevant cells that express disease-relevant markers. The specific aim of the study was to develop a convenient and reliable method for screening compounds with Tumor Necrosis Factor-alpha (TNF-α) inhibitory activity. This assay was developed using cryopreserved ready-to-use cartilage-derived cells isolated from juvenile donors diagnosed with polydactyly. It has been demonstrated that all donor (10 donors) cells were able to respond to TNF-α treatment by increased secretion of pro-inflammatory cytokine IL-6 into subcultural medium. Inhibition of TNF-α using commercially available TNF-α inhibitor etanercept resulted in a dose-dependent decrease in IL-6 production which was measured by Enzyme-Linked Immunosorbent Assay (ELISA). TNF-α dependent IL-6 production was detected in the cells after both their prolonged cultivation in vitro (≥20 passages) and cryopreservation. This phenotypic bioassay based on ready-to-use primary human cells was developed for detection of novel TNF-α inhibitory compounds and profiling of biosimilar drugs. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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Review

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18 pages, 361 KiB  
Review
Endothelial Dysfunction and Extra-Articular Neurological Manifestations in Rheumatoid Arthritis
by Jessica Maiuolo, Carolina Muscoli, Micaela Gliozzi, Vincenzo Musolino, Cristina Carresi, Sara Paone, Sara Ilari, Rocco Mollace, Ernesto Palma and Vincenzo Mollace
Biomolecules 2021, 11(1), 81; https://doi.org/10.3390/biom11010081 - 10 Jan 2021
Cited by 24 | Viewed by 4506
Abstract
Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory autoimmune disease that affects about 1% of the global population, with a female–male ratio of 3:1. RA preferably affects the joints, with consequent joint swelling and deformities followed by ankylosis. However, evidence has accumulated showing [...] Read more.
Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory autoimmune disease that affects about 1% of the global population, with a female–male ratio of 3:1. RA preferably affects the joints, with consequent joint swelling and deformities followed by ankylosis. However, evidence has accumulated showing that patients suffering from RA can also develop extra-articular manifestations, including cardiovascular disease states, neuropathies, and multiorgan dysfunction. In particular, peripheral nerve disorders showed a consistent impact in the course of the disease (prevalence about 20%) mostly associated to vasculitis of the nerve vessels leading to vascular ischemia, axonal degeneration, and neuronal demyelination. The pathophysiological basis of this RA-associated microvascular disease, which leads to impairment of assonal functionality, is still to be better clarified. However, endothelial dysfunction and alterations of the so-called brain-nerve barrier (BNB) seem to play a fundamental role. This review aims to assess the potential mechanisms underlying the impairment of endothelial cell functionality in the development of RA and to identify the role of dysfunctional endothelium as a causative mechanism of extra-articular manifestation of RA. On the other hand, the potential impact of lifestyle and nutritional interventions targeting the maintenance of endothelial cell integrity in patients with RA will be discussed as a potential option when approaching therapeutic solutions in the course of the disease. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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18 pages, 3426 KiB  
Review
Rheumatoid Arthritis in the View of Osteoimmunology
by Mélanie Auréal, Irma Machuca-Gayet and Fabienne Coury
Biomolecules 2021, 11(1), 48; https://doi.org/10.3390/biom11010048 - 31 Dec 2020
Cited by 64 | Viewed by 6220
Abstract
Rheumatoid arthritis is characterized by synovial inflammation and irreversible bone erosions, both highlighting the immense reciprocal relationship between the immune and bone systems, designed osteoimmunology two decades ago. Osteoclast-mediated resorption at the interface between synovium and bone is responsible for the articular bone [...] Read more.
Rheumatoid arthritis is characterized by synovial inflammation and irreversible bone erosions, both highlighting the immense reciprocal relationship between the immune and bone systems, designed osteoimmunology two decades ago. Osteoclast-mediated resorption at the interface between synovium and bone is responsible for the articular bone erosions. The main triggers of this local bone resorption are autoantibodies directed against citrullinated proteins, as well as pro-inflammatory cytokines and the receptor activator of nuclear factor-κB ligand, that regulate both the formation and activity of the osteoclast, as well as immune cell functions. In addition, local bone loss is due to the suppression of osteoblast-mediated bone formation and repair by inflammatory cytokines. Similarly, inflammation affects systemic bone remodeling in rheumatoid arthritis with the net increase in bone resorption, leading to systemic osteoporosis. This review summarizes the substantial progress that has been made in understanding the pathophysiology of systemic and local bone loss in rheumatoid arthritis. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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24 pages, 1321 KiB  
Review
Biomarkers to Personalize the Treatment of Rheumatoid Arthritis: Focus on Autoantibodies and Pharmacogenetics
by Valeria Conti, Graziamaria Corbi, Maria Costantino, Emanuela De Bellis, Valentina Manzo, Carmine Sellitto, Berenice Stefanelli, Francesca Colucci and Amelia Filippelli
Biomolecules 2020, 10(12), 1672; https://doi.org/10.3390/biom10121672 - 14 Dec 2020
Cited by 16 | Viewed by 4854
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease that is very complex and heterogeneous. If not adequately treated, RA patients are likely to manifest excess of morbidity and disability with an important impact on the quality of life. Pharmacological treatment is based on [...] Read more.
Rheumatoid arthritis (RA) is a chronic inflammatory disease that is very complex and heterogeneous. If not adequately treated, RA patients are likely to manifest excess of morbidity and disability with an important impact on the quality of life. Pharmacological treatment is based on the administration of the disease-modifying antirheumatic drugs (DMARDs), subdivided into conventional synthetic (csDMARDs), targeted synthetic (tsDMARDs), and biological (bDMARDs). bDMARDs are now frequently administered in patients, both as alternative treatment and together with csDMARDs. Unfortunately, there is a therapeutic response variability both to old and new drugs. Therefore, to identify pre-therapeutic and on-treatment predictors of response is a priority. This review aims to summarize recent advances in understanding the causes of the variability in treatment response in RA, with particular attention to predictive potential of autoantibodies and DMARD pharmacogenetics. In recent years, several biomarkers have been proposed to personalize the therapy. Unfortunately, a magic bullet does not exist, as many factors concur to disease susceptibility and treatment outcomes, acting around the patient’s congenital background. Models integrating demographic, clinical, biochemical, and genetic data are needed to enhance the predictive capacity of specific factors singularly considered to optimize RA treatment in light of multidisciplinary patient management. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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23 pages, 3003 KiB  
Review
DMARDs–Gut Microbiota Feedback: Implications in the Response to Therapy
by Oscar Zaragoza-García, Natividad Castro-Alarcón, Gloria Pérez-Rubio and Iris Paola Guzmán-Guzmán
Biomolecules 2020, 10(11), 1479; https://doi.org/10.3390/biom10111479 - 24 Oct 2020
Cited by 20 | Viewed by 4358
Abstract
Due to its immunomodulatory effects and the limitation in the radiological damage progression, disease-modifying antirheumatic drugs (DMARDs) work as first-line rheumatoid arthritis (RA) treatment. In recent years, numerous research projects have suggested that the metabolism of DMARDs could have a role in gut [...] Read more.
Due to its immunomodulatory effects and the limitation in the radiological damage progression, disease-modifying antirheumatic drugs (DMARDs) work as first-line rheumatoid arthritis (RA) treatment. In recent years, numerous research projects have suggested that the metabolism of DMARDs could have a role in gut dysbiosis, which indicates that the microbiota variability could modify the employment of direct and indirect mechanisms in the response to treatment. The main objective of this review was to understand the gut microbiota bacterial variability in patients with RA, pre and post-treatment with DMARDs, and to identify the possible mechanisms through which microbiota can regulate the response to pharmacological therapy. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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22 pages, 879 KiB  
Review
Amino Acid Metabolism in Rheumatoid Arthritis: Friend or Foe?
by Eleonora Panfili, Roberto Gerli, Ursula Grohmann and Maria Teresa Pallotta
Biomolecules 2020, 10(9), 1280; https://doi.org/10.3390/biom10091280 - 4 Sep 2020
Cited by 33 | Viewed by 5740
Abstract
In mammals, amino acid metabolism has evolved to act as a critical regulator of innate and adaptive immune responses. Rheumatoid arthritis (RA) is the most common form of inflammatory arthropathy sustained by autoimmune responses. We examine here the current knowledge of tryptophan and [...] Read more.
In mammals, amino acid metabolism has evolved to act as a critical regulator of innate and adaptive immune responses. Rheumatoid arthritis (RA) is the most common form of inflammatory arthropathy sustained by autoimmune responses. We examine here the current knowledge of tryptophan and arginine metabolisms and the main immunoregulatory pathways in amino acid catabolism, in both RA patients and experimental models of arthritis. We found that l-tryptophan (Trp) metabolism and, in particular, the kynurenine pathway would exert protective effects in all experimental models and in some, but not all, RA patients, possibly due to single nucleotide polymorphisms in the gene coding for indoleamine 2,3-dioxygenase 1 (IDO1; the enzyme catalyzing the rate-limiting step of the kynurenine pathway). The function, i.e., either protective or pathogenetic, of the l-arginine (Arg) metabolism in RA was less clear. In fact, although immunoregulatory arginase 1 (ARG1) was highly induced at the synovial level in RA patients, its true functional role is still unknown, possibly because of few available preclinical data. Therefore, our analysis would indicate that amino acid metabolism represents a fruitful area of research for new drug targets for a more effective and safe therapy of RA and that further studies are demanding to pursue such an important objective. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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11 pages, 270 KiB  
Review
Polymorphisms Involved in Response to Biological Agents Used in Rheumatoid Arthritis
by Giovanni Pallio, Federica Mannino, Natasha Irrera, Ali H. Eid, Francesco Squadrito and Alessandra Bitto
Biomolecules 2020, 10(9), 1203; https://doi.org/10.3390/biom10091203 - 19 Aug 2020
Cited by 10 | Viewed by 3012
Abstract
Rheumatoid arthritis (RA) is a systemic disease that leads to joint destruction. During the last decade, the therapy of RA has been principally based on biological drugs. Although the efficacy of biological therapy has been established, patients demonstrated a high heterogeneity in clinical [...] Read more.
Rheumatoid arthritis (RA) is a systemic disease that leads to joint destruction. During the last decade, the therapy of RA has been principally based on biological drugs. Although the efficacy of biological therapy has been established, patients demonstrated a high heterogeneity in clinical response to treatment. Several genetic polymorphisms play a part in the different response to biological drugs. This review summarizes the pharmacogenetics of biological agents approved for clinical RA treatment. We reviewed PubMed papers published over the past 20 years (2000–2020), inserting as the search term “rheumatoid arthritis and polymorphisms”. Despite some studies showing important correlations between genetic polymorphisms and response to biological therapy in RA patients, most of these findings are still lacking and inconsistent. The personalized treatment according to a pharmacogenetics approach is promising but the available pharmacogenetics data on biological treatment in RA are not adequate and reliable to recommend pharmacogenetic tests before starting biological therapy in RA patients. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
40 pages, 1674 KiB  
Review
JAK-Inhibitors for the Treatment of Rheumatoid Arthritis: A Focus on the Present and an Outlook on the Future
by Jacopo Angelini, Rossella Talotta, Rossana Roncato, Giulia Fornasier, Giorgia Barbiero, Lisa Dal Cin, Serena Brancati and Francesco Scaglione
Biomolecules 2020, 10(7), 1002; https://doi.org/10.3390/biom10071002 - 5 Jul 2020
Cited by 120 | Viewed by 14247
Abstract
Janus kinase inhibitors (JAKi) belong to a new class of oral targeted disease-modifying drugs which have recently revolutionized the therapeutic panorama of rheumatoid arthritis (RA) and other immune-mediated diseases, placing alongside or even replacing conventional and biological drugs. JAKi are characterized by a [...] Read more.
Janus kinase inhibitors (JAKi) belong to a new class of oral targeted disease-modifying drugs which have recently revolutionized the therapeutic panorama of rheumatoid arthritis (RA) and other immune-mediated diseases, placing alongside or even replacing conventional and biological drugs. JAKi are characterized by a novel mechanism of action, consisting of the intracellular interruption of the JAK-STAT pathway crucially involved in the immune response. The aim of this narrative review is to globally report the most relevant pharmacological features and clinical outcomes of the developed and incoming JAKi for RA, based on the available preclinical and clinical evidence. A total of 219 papers, including narrative and systematic reviews, randomized controlled trials (RCTs), observational studies, case reports, guidelines, and drug factsheets, were selected. The efficacy and safety profile of both the first generation JAKi (baricitinib and tofacitinib) and the second generation JAKi (upadacitinib, filgotinib, peficitinib, decernotinib and itacitinib) were compared and discussed. Results from RCTs and real-life data are encouraging and outline a rapid onset of the pharmacologic effects, which are maintained during the time. Their efficacy and safety profile are comparable or superior to those of biologic agents and JAKi proved to be efficacious when given as monotherapy. Finally, the manufacturing of JAKi is relatively easier and cheaper than that of biologics, thus increasing the number of compounds being formulated and tested for clinical use. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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10 pages, 1201 KiB  
Brief Report
Over-Expression of Allograft Inflammatory Factor-1 (AIF-1) in Patients with Rheumatoid Arthritis
by Katarzyna Piotrowska, Sylwia Słuczanowska-Głabowska, Mateusz Kurzawski, Violetta Dziedziejko, Patrycja Kopytko, Edyta Paczkowska, Dorota Rogińska, Krzysztof Safranow, Bogusław Machaliński and Andrzej Pawlik
Biomolecules 2020, 10(7), 1064; https://doi.org/10.3390/biom10071064 - 16 Jul 2020
Cited by 18 | Viewed by 2787
Abstract
Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic protein that is encoded by the AIF1 gene. The main functions of AIF-1 are the activation of macrophages and enhancing the production of pro-inflammatory cytokines. To date, three different AIF-1 isoforms have been identified. In this [...] Read more.
Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic protein that is encoded by the AIF1 gene. The main functions of AIF-1 are the activation of macrophages and enhancing the production of pro-inflammatory cytokines. To date, three different AIF-1 isoforms have been identified. In this study, we examined the expression of AIF-1 isoforms on the level of mRNA, and we compared the percentage of AIF-1-positive white blood cells (WBCs) in blood and AIF-1/CD68 cells in the synovial membranes in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). We examined 15 patients with RA and 15 patients with OA who had previously undergone knee arthroplasty. Peripheral blood and synovial membranes (SMs) were collected from these patients during knee arthroplasty. We identified three AIF-1 mRNA expression variants in peripheral mononuclear cells (PBMCs) and SMs from patients in both groups. Spearman’s rank correlation coefficient tests showed strong, positive, and significant correlations between the three AIF-1 mRNA expression variants in PBMCs and/or SMs in patients with RA and OA. There were no statistically significant correlations for any of the AIF-1 mRNA expression variants between PBMCs and SMs in patients with RA and OA. We observed a statistically significant increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The percentage of AIF-1-positive cells in the blood of patients with RA and OA was 1.35 ± 0.81% and 0.71 ± 0.25% (p < 0.01), respectively, whereas the percentage of AIF-1/CD68-positive WBC cells in the SMs was 24.05 ± 7.17% and 4.78 ± 1.52% (p < 0.001), respectively. In conclusion, three AIF-1 mRNA expression variants occurred in PBMCs and SM cells in patients with RA and OA. The AIF-1 mRNA expression levels of the variants correlated with each other in PBMCs and SM cells, but there were no statistically significant correlations for AIF-1 mRNA expression variants between PBMCs and SM cells in patients with RA and OA. Both in the blood and SMs, we observed an increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The above results suggested that AIF-1 was the cytokine involved in the pathogenesis of RA. The precise knowledge of the role of AIF-1 in RA pathogenesis and the development of inflammatory response requires further investigations. Full article
(This article belongs to the Special Issue Pathogenesis of Arthritis)
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