TNF-αpotentiates uric acid-induced interleukin-1β(IL-1β) secretion in human neutrophils

Yokose, Kohei; Sato, Shuzo; Asano, Tomohiko; Yashiro, Makiko; Kobayashi, Hiroko; Watanabe, Hiroshi; Suzuki, Eiji; Sato, Chikako; Kozuru, Hideko; Yatsuhashi, Hiroshi; Migita, Kiyoshi

doi:10.1080/14397595.2017.1369924

Cited by 42 publications

(34 citation statements)

References 28 publications

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“…Various stimuli are able to prime monocytes/macrophages for inflammasome activation by pathogenic crystals. Indeed, priming with serum amyloid A (SAA), TLR ligands, or TNF warranted the capacity of MSU to activate the inflammasome and induce release of IL‐1β in human cells . Of interest, also soluble uric acids were able to deliver the priming signal; however, the precipitation of uric acid into MSU crystals was necessary for NLRP3 inflammasome activity .…”

Section: Inflammasome In Gouty Arthritismentioning

confidence: 99%

“…Indeed, priming with serum amyloid A (SAA), TLR ligands, or TNF warranted the capacity of MSU to activate the inflammasome and induce release of IL-1β in human cells. [104][105][106][107][108] Of interest, also soluble uric acids were able to deliver the priming signal 109,110 ; however, the precipitation of uric acid into MSU crystals was necessary for NLRP3 inflammasome activity. 110 These results suggest that hyperuricemia, the condition of elevated systemic uric acid levels that precedes gout pathology, may provide the priming signal that sets of inflammasome activation once MSU crystals are formed and deposited.…”

Section: Infl Amma Some In Gout Y Arthritismentioning

confidence: 99%

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Inflammasomes contributing to inflammation in arthritis

Spel

Martinon

2020

Immunological Reviews

126

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Inflammasomes are intracellular multiprotein signaling platforms that initiate inflammatory responses in response to pathogens and cellular damage. Active inflammasomes induce the enzymatic activity of caspase‐1, resulting in the induction of inflammatory cell death, pyroptosis, and the maturation and secretion of inflammatory cytokines IL‐1β and IL‐18. Inflammasomes are activated in many inflammatory diseases, including autoinflammatory disorders and arthritis, and inflammasome‐specific therapies are under development for the treatment of inflammatory conditions. In this review, we outline the different inflammasome platforms and recent findings contributing to our knowledge about inflammasome biology in health and disease. In particular, we discuss the role of the inflammasome in the pathogenesis of arthritic diseases, including rheumatoid arthritis, gout, ankylosing spondylitis, and juvenile idiopathic arthritis, and the potential of newly developed therapies that specifically target the inflammasome or its products for the treatment of inflammatory diseases.

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Section: Inflammasome In Gouty Arthritismentioning

confidence: 99%

Section: Infl Amma Some In Gout Y Arthritismentioning

confidence: 99%

Inflammasomes contributing to inflammation in arthritis

Spel

Martinon

2020

Immunological Reviews

126

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“…Similarly, in mice deficient for TNF-α or its receptors, in addition to decreased pain induced by MSU, inhibition of neutrophil infiltration and production of CXCL1 and IL-1β occurs (Amaral et al, 2016). TNF-α also primes human neutrophils in a manner that these leukocytes start to respond to previously inactive concentrations of MSU as observed by IL-1β secretion (Yokose et al, 2017). Complex I inhibited MSU-induced production of pro-inflammatory cytokines TNF-α and IL-6.…”

Section: Discussionmentioning

confidence: 99%

[Ru(bpy)2(NO)SO3](PF6), a Nitric Oxide Donating Ruthenium Complex, Reduces Gout Arthritis in Mice

et al. 2019

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Monosodium urate crystals (MSU) deposition induces articular inflammation known as gout. This disease is characterized by intense articular inflammation and pain by mechanisms involving the activation of the transcription factor NFκB and inflammasome resulting in the production of cytokines and oxidative stress. Despite evidence that MSU induces iNOS expression, there is no evidence on the effect of nitric oxide (NO) donors in gout. Thus, the present study evaluated the effect of the ruthenium complex donor of NO {[Ru(bpy)2(NO)SO3](PF6)} (complex I) in gout arthritis. Complex I inhibited in a dose-dependent manner MSU-induced hypersensitivity to mechanical stimulation, edema and leukocyte recruitment. These effects were corroborated by a decrease of histological inflammation score and recruitment of Lysm-eGFP+ cells. Mechanistically, complex I inhibited MSU-induced mechanical hypersensitivity and joint edema by triggering the cGMP/PKG/ATP-sensitive K (+) channels signaling pathway. Complex I inhibited MSU-induced oxidative stress and pro-inflammatory cytokine production in the knee joint. These data were supported by the observation that complex I inhibited MSU-induced NFκB activation, and IL-1β expression and production. Complex I also inhibited MSU-induced activation of pro-IL-1β processing. Concluding, the present data, to our knowledge, is the first evidence that a NO donating ruthenium complex inhibits MSU-induced articular inflammation and pain. Further, complex I targets the main physiopathological mechanisms of gout arthritis. Therefore, it is envisaged that complex I and other NO donors have therapeutic potential that deserves further investigation.

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“…Tumor Necrosis Factor-ɑ (TNF-ɑ) is a proinflammatory cytokine mediating inflammation and apoptosis [ 129 ]. A promoter region SNP of the TNF-A gene rs1800630 (-863C/A) was associated with gout in a male Chinese cohort [ 130 ].…”

Section: Tnf-a Mcp-1/ccl2 Nlrp3 Ppargc1b Tlr4 Card8 and P2x7rmentioning

confidence: 99%

Multiple Membrane Transporters and Some Immune Regulatory Genes are Major Genetic Factors to Gout

2018

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Gout is a common form of inflammatory arthritis caused by hyperuricemia and the deposition of Monosodium Urate (MSU) crystals. It is also considered as a complex disorder in which multiple genetic factors have been identified in association with its susceptibility and/or clinical outcomes. Major genes that were associated with gout include URAT1, GLUT9, OAT4, NPT1 (SLC17A1), NPT4 (SLC17A3), NPT5 (SLC17A4), MCT9, ABCG2, ABCC4, KCNQ1, PDZK1, NIPAL1, IL1β, IL-8, IL-12B, IL-23R, TNFA, MCP-1/CCL2, NLRP3, PPARGC1B, TLR4, CD14, CARD8, P2X7R, EGF, A1CF, HNF4G and TRIM46, LRP2, GKRP, ADRB3, ADH1B, ALDH2, COMT, MAOA, PRKG2, WDR1, ALPK1, CARMIL (LRRC16A), RFX3, BCAS3, CNIH-2, FAM35A and MYL2-CUX2. The proteins encoded by these genes mainly function in urate transport, inflammation, innate immunity and metabolism. Understanding the functions of gout-associated genes will provide important insights into future studies to explore the pathogenesis of gout, as well as to develop targeted therapies for gout.

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TNF-αpotentiates uric acid-induced interleukin-1β(IL-1β) secretion in human neutrophils

Abstract: Our data demonstrate that priming of human neutrophils with TNF-α promotes uric acid-mediated IL-1β secretion in the absence of microbial stimulation. These findings provide insights into the neutrophils-mediated inflammatory processes in gouty arthritis.

Cited by 42 publications

References 28 publications

Inflammasomes contributing to inflammation in arthritis

Inflammasomes contributing to inflammation in arthritis

[Ru(bpy)2(NO)SO3](PF6), a Nitric Oxide Donating Ruthenium Complex, Reduces Gout Arthritis in Mice

Multiple Membrane Transporters and Some Immune Regulatory Genes are Major Genetic Factors to Gout

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