ArticleArthritis research & therapy2019
Hydroxychloroquine inhibits IL-1β production from amyloid-stimulated human neutrophils.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Trial
- Hydroxychloroquine-induced Retinal Toxicity.Frontiers in pharmacology · 2023Review
- Effects of Drugs Formerly Suggested for COVID-19 Repurposing on Pannexin1 Channels.International journal of molecular sciences · 2022Article
- Review
- Antimalarials - old drugs are new again.Postepy dermatologii i alergologii · 2022Review
- MicroRNA-140-5p represses chondrocyte pyroptosis and relieves cartilage injury in osteoarthritis by inhibiting cathepsin B/Nod-like receptor protein 3.Bioengineered · 2021Article
- Article
- Electrospun Polydioxanone Loaded With Chloroquine Modulates Template-Induced NET Release and Inflammatory Responses From Human Neutrophils.Frontiers in bioengineering and biotechnology · 2021Article
- Evaluation of mechanisms of action of re-purposed drugs for treatment of COVID-19.Cellular immunology · 2020Review
- NLRP3 Inflammasome: The Stormy Link Between Obesity and COVID-19.Frontiers in immunology · 2020Review
- Targeting Neutrophils to Treat Acute Respiratory Distress Syndrome in Coronavirus Disease.Frontiers in pharmacology · 2020Review
- SARS-CoV-2: Pathogenesis, and Advancements in Diagnostics and Treatment.Frontiers in immunology · 2020Review
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Authors and funding
15 authors.
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Abstract
backgroundHydroxychloroquine (HCQ) is used for the treatment of patients with rheumatic diseases. We tested the hypothesis that HCQ affects the NLRP3 inflammasome, which is involved in autoinflammation.
methodsHuman neutrophils were stimulated with serum amyloid A (SAA) in vitro and measured for IL-1β and caspase-1 (p20) secretion by ELISA. Pro-IL-1β mRNA expression in human neutrophils was quantified by real-time RT-PCR.
resultsSAA stimulation induced significant production of IL-1β in human neutrophils. SAA stimulation also induced NF-κB activation, pro-IL-1β mRNA expression, and NLRP3 protein expression in human neutrophils. HCQ pretreatment significantly inhibited the SAA-induced IL-1β production in human neutrophils, but did not affect the SAA-induced NF-κB activation, pro-IL-1β mRNA expression, and NLRP3 protein expression. Furthermore, SAA stimulation induced cleaved caspase-1 (p20) secretion from human neutrophils, and this release was suppressed by HCQ pretreatment.
conclusionsTreatment with HCQ was associated with impaired production of IL-1β in SAA-stimulated human neutrophils without affecting the priming process of the NLRP3 inflammasome such as pro-IL-1β or NLRP3 induction. These findings suggest that HCQ affects the NLRP3 activation process, resulting in the impaired IL-1β production in human neutrophils, as representative innate immune cells.
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