The role of interleukin-1 family members in hyperuricemia and gout

Klück, Viola; Liu, Rui-qi; Joosten, Leo A. B.

doi:10.1016/j.jbspin.2020.105092

Cited by 47 publications

(29 citation statements)

References 54 publications

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“…IL-33, IL-37, and IL-38 have an inhibitory function in MSU crystal-induced inflammation. Furthermore, IL-37 regulates uric acid metabolism by affecting the protein level of PDZK1, a cytoskeletal controller of uric acid transport [ 24 , 25 ].…”

Section: Molecular Mechanisms Of Gouty Inflammationmentioning

confidence: 99%

Autoinflammatory Features in Gouty Arthritis

Galozzi

Bindoli

Doria

et al. 2021

JCM

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In the panorama of inflammatory arthritis, gout is the most common and studied disease. It is known that hyperuricemia and monosodium urate (MSU) crystal-induced inflammation provoke crystal deposits in joints. However, since hyperuricemia alone is not sufficient to develop gout, molecular-genetic contributions are necessary to better clinically frame the disease. Herein, we review the autoinflammatory features of gout, from clinical challenges and differential diagnosis, to the autoinflammatory mechanisms, providing also emerging therapeutic options available for targeting the main inflammatory pathways involved in gout pathogenesis. This has important implication as treating the autoinflammatory aspects and not only the dysmetabolic side of gout may provide an effective and safer alternative for patients even in the prevention of possible gouty attacks.

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Section: Molecular Mechanisms Of Gouty Inflammationmentioning

confidence: 99%

Autoinflammatory Features in Gouty Arthritis

Galozzi

Bindoli

Doria

et al. 2021

JCM

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“…IL-6 is a vital mediator of cartilage degeneration, inflammatory cell aggregation and inflammatory reaction sustainability. TNF-α is mainly produced by activated macrophages in GA patients, and is a key factor leading to inflammatory reactions and joint destruction [ 30 ]. The inflammatory factors in mice ankle joints and THP-1-derived macrophage supernatants were detected by ELISA kits.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways

Zhang

et al. 2022

Molecules

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Gouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of Smilax glabra, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in treating GA has not yet been clarified. Thus, this study was to investigate the protective effects of neoastilbin in both monosodium urate (MSU) stimulated THP-1-derived macrophages and the animal model of GA by injecting MSU into the ankle joints of mice. The levels of key inflammatory cytokines in MSU stimulated THP-1-derived macrophages were detected by enzyme-linked immunosorbent assay (ELISA) kits. Protein expressions of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome pathways were further detected by Western blotting. In addition, swelling degree of ankle joints, the levels of inflammatory factors, infiltration of inflammatory cells and the expressions of related proteins were determined. Swelling degree and histopathological injury in ankle joints of MSU-injected mice were significantly decreased after being treated with neoastilbin. Moreover, neoastilbin significantly diminished the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), suppressing the activation of NF-κB and NLRP3 inflammasome pathways in both MSU stimulated THP-1-derived macrophages and the mouse model of GA. In summary, neoastilbin could alleviate GA by inhibiting the NF-κB and NLRP3 inflammasome pathways, which provided some evidence for neoastilbin as a promising therapeutic agent for GA treatment.

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“…As reviewed in this study, alterations in serum levels of IL-38 played a major role in the immunopathogenesis of many diseases, in which patients had been previously faced with a wide array of problems due to the lack of prognosis or accurate diagnosis and improper treatment [213][214][215][216][217][218][219][220][221]. At the time of the literature review for this systematic review study, as there is a global pandemic of Coronavirus, it has been demonstrated that anti-inflammatory properties of IL-38 can be considered as recently-emerged pharmacotherapies for alleviation of the inflammatory symptoms of patients with SARS-CoV-2 infection [186,222].…”

Section: Future Directions and Conclusionmentioning

confidence: 99%

Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study

Esmaeilzadeh

Bahmaie

Nouri

et al. 2021

IJMS

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Exponential growth in the usage of “cytokines” (as seroimmunobiomarkers) has facilitated more accurate prognosis, early diagnosis, novel, and efficient immunotherapeutics. Numerous studies have reported immunopathophysiological and immunopathological processes of interleukin-38 (IL-38). Therefore, in this systematic review article, the authors aimed to present an updated comprehensive overview on the immunobiological mechanisms, diagnostic, and immune gene-based therapeutic potentials of IL-38. According to our inclusion and exclusion criteria, a total of 216 articles were collected from several search engines and databases from the January 2012 to July 2021 time interval by using six main keywords. Physiologic or pathologic microenvironments, optimal dosage, and involved receptors affect the functionalities of IL-38. Alterations in serum levels of IL-38 play a major role in the immunopathogenesis of a wide array of immune-mediated disorders. IL-38 shows anti-inflammatory activities by reduction or inhibition of pro-inflammatory cytokines, supporting the therapeutic aspects of IL-38 in inflammatory autoimmune diseases. According to the importance of pre-clinical studies, it seems that manipulation of the immune system by immunomodulatory properties of IL-38 can increase the accuracy of diagnosis, and decipher optimal clinical outcomes. To promote our knowledge, more collaboration is highly recommended among laboratory scientists, internal/infectious diseases specialists, oncologists, immunologists, diseases-specific biomarkers scientists, and basic medical researchers.

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The role of interleukin-1 family members in hyperuricemia and gout

Cited by 47 publications

References 54 publications

Autoinflammatory Features in Gouty Arthritis

Autoinflammatory Features in Gouty Arthritis

The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways

Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study

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