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

• Published in: Modern rheumatology Vol. 28; no. 3; pp. 513 - 517
• Main Authors: Yokose, Kohei, Sato, Shuzo, Asano, Tomoyuki, Yashiro, Makiko, Kobayashi, Hiroko, Watanabe, Hiroshi, Suzuki, Eiji, Sato, Chikako, Kozuru, Hideko, Yatsuhashi, Hiroshi, Migita, Kiyoshi
• Format: Journal Article
• Language: English
• Published: United States 01.05.2018
• Subjects: Arthritis, Gouty - metabolism; Cells, Cultured; Humans; Interleukin-1beta - metabolism; Neutrophils - drug effects; Neutrophils - metabolism; Tumor Necrosis Factor-alpha - pharmacology; Uric Acid - pharmacology; TNF-α; monosodium urate; IL-1β; inflammasome; gout; Caspase-1
• ISSN: 1439-7595; 1439-7609
• DOI: 10.1080/14397595.2017.1369924

Monosodium urate (MSU) has been shown to promote interleukin-1β (IL-1β) secretion in human monocytes, but the priming signals for NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome pathway remains elusive. In this study, we investigated the role of Tumor necrosis factor-alpha (TNF-α) on MSU-mediated IL-1β induction in human neutrophils. Human neutrophils were stimulated with MSU, in the presence or absence of TNF-α priming. The cellular supernatants were analyzed for IL-1β, IL-18, and caspase-1 by enzyme-linked immunosorbent assay (ELISA) methods. Pro-IL-1β mRNA expressions in human neutrophils were analyzed by real-time PCR method. TNF-α stimulation induced pro-IL-1β mRNA expression; however, MSU stimulation did not induce pro-IL-1β mRNA expression in human neutrophils. TNF-α alone or MSU stimulation did not result in efficient IL-1β secretion in human neutrophils, whereas in TNF-α-primed neutrophils, MSU stimulation resulted in a marked IL-1β and IL-18 secretion. TNF-α-primed neutrophils secreted cleaved caspase-1 (p20), in response to MSU stimulation. 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.