Profile of serum cytokine concentrations in patients with gouty arthritis

Zhang, Tie; Wang, Guozhen; Zheng, Jun; Li, Shirui; Xu, Jing

doi:10.1177/03000605211055618

Cited by 12 publications

(9 citation statements)

References 26 publications

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“…However, we did not find increased numbers of circulating IFN-g + T cells in gout condition (Fig. 4), consistent with recent reports (114,115). Similarly, we did not find significant differences in IL-17-production by T cells (data not shown), despite previous studies reporting increased levels of Th17-related cytokines in gout (41,42).…”

Section: Discussionsupporting

confidence: 92%

Peripheral T cell populations are differentially affected in monogenic autoinflammatory syndromes and gout

Al¹,

Bruno²,

Röring³

et al. 2023

Preprint

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Purpose Both monogenic autoinflammatory syndromes, such as Chronic Granulomatous Disease (CGD) and Familial Mediterranean Fever (FMF), and the common inflammatory disease gout are characterized by episodes of sterile inflammatory attacks in the absence of an infection. While these disorders encompass distinct pathologies due to differentially affected metabolic pathways and inflammasome activation mechanisms, their common features are the excessive production of interleukin (IL)-1ß and innate immune cell hyperreactivity. On the other hand, the role of T cells and innate-like lymphocytes such as gamma delta (γδ) T cells in these pathologies is ill-defined. Methods In order to widen our understanding of T cell involvement in FMF, CGD and gout pathology we developed multicolour immunophenotyping panels for flow cytometry and functional assays to characterise gd T cells, as well as CD4 and CD8 T cell populations in terms of their cytokine production, activation status, memory or naive phenotypes, exhaustion status, homing receptor expression, and cytotoxic activity. Results Our study is the first deep immunophenotyping analysis of T cell populations in FMF, CGD and gout patients. We found that CGD affects the frequencies and activation status of T cells, while gout impairs cytokine production capacity of Vd2 T cells and reshapes homing receptor expression by T cells. FMF was characterized by only minor effects on T cell populations. Conclusion Autoinflammatory syndromes differentially affect T cell compartments. Future studies are warranted to assess whether these phenotypical changes are relevant for disease pathology.

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Section: Discussionsupporting

confidence: 92%

Peripheral T cell populations are differentially affected in monogenic autoinflammatory syndromes and gout

Al¹,

Bruno²,

Röring³

et al. 2023

Preprint

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show abstract

“…A study of 91 participants showed that serum IFN-g is not elevated in hyperuricemia and gout patients (43), which contrasts another recent study of 240 participants showing that IFN-g is significantly elevated in the gout remission stage (44). Therefore, these seemingly contradictory results demand further investigation.…”

Section: Discussionmentioning

confidence: 83%

Purine-Induced IFN-γ Promotes Uric Acid Production by Upregulating Xanthine Oxidoreductase Expression

et al. 2022

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ObjectiveLimiting purine intake, inhibiting xanthine oxidoreductase (XOR) and inhibiting urate reabsorption in proximal tubule by uricosuric drugs, to reduce serum uric acid (UA) levels, are recognized treatments for gout. However, the mechanism of increased how XOR expression and activity in hyperuricemia and gout remains unclear. This study aims to explore whether exogenous purines are responsible for increased XOR expression and activity.MethodsHepG2 and Bel-7402 human hepatoma cells were stimulated with exogenous purine, or were exposed to conditioned growth medium of purine-stimulated Jurkat cells, followed by measurement of XOR expression and UA production to determine the effect of lymphocyte-secreted cytokines on XOR expression in hepatocytes. The expression of STAT1, IRF1 and CBP and their binding on the XDH promoter were detected by western blotting and ChIP-qPCR. The level of DNA methylation was determined by bisulfite sequencing PCR. Blood samples from 117 hyperuricemia patients and 119 healthy individuals were collected to analyze the correlation between purine, UA and IFN-γ concentrations.ResultsExcess of purine was metabolized to UA in hepatocyte metabolism by XOR that was induced by IFN-γ secreted in the conditioned growth medium of Jurkat cells in response to exogenous purine, but it did not directly induce XOR expression. IFN-γ upregulated XOR expression due to the enhanced binding of STAT1 to IRF1 to further recruit CBP to the XDH promoter. Clinical data showed positive correlation of serum IFN‐γ with both purine and UA, and associated risk of hyperuricemia.ConclusionPurine not only acts as a metabolic substrate of XOR for UA production, but it induces inflammation through IFN-γ secretion that stimulates UA production through elevation of XOR expression.

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“…Studies have shown that IL-6 is associated with the presence of gouty stones and joint deformities and serves as a prognostic indicator of disease progression in gout. 33,34 Moreover, it was demonstrated that IL-6 induced osteoclast formation. 35 Wenjing Xu et al 36 found that reducing IL-6 secretion through drug intervention could alleviate the symptoms of gout flare.…”

Section: Jak/stat Signaling Pathwaymentioning

confidence: 99%

Pathogenesis of gout: Exploring more therapeutic target

Xiao,

Xie,

et al. 2024

Int J of Rheum Dis

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Gout is a chronic metabolic and immune disease, and its specific pathogenesis is still unclear. When the serum uric acid exceeds its saturation in the blood or tissue fluid, it is converted to monosodium urate crystals, which lead to acute arthritis of varying degrees, urinary stones, or irreversible peripheral joint damage, and in severe cases, impairment of vital organ function. Gout flare is a clinically significant state of acute inflammation in gout. The current treatment is mostly anti‐inflammatory analgesics, which have numerous side effects with limited treatment methods. Gout pathogenesis involves many aspects. Therefore, exploring gout pathogenesis from multiple perspectives is conducive to identifying more therapeutic targets and providing safer and more effective alternative treatment options for patients with gout flare. Thus, this article is of great significance for further exploring the pathogenesis of gout. The author summarizes the pathogenesis of gout from four aspects: signaling pathways, inflammatory factors, intestinal flora, and programmed cell death, focusing on exploring more new therapeutic targets.

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Profile of serum cytokine concentrations in patients with gouty arthritis

Cited by 12 publications

References 26 publications

Peripheral T cell populations are differentially affected in monogenic autoinflammatory syndromes and gout

Peripheral T cell populations are differentially affected in monogenic autoinflammatory syndromes and gout

Purine-Induced IFN-γ Promotes Uric Acid Production by Upregulating Xanthine Oxidoreductase Expression

Pathogenesis of gout: Exploring more therapeutic target

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