scholarly journals Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation

2011 ◽  
Vol 108 (5) ◽  
pp. 2088-2093 ◽  
Author(s):  
Anna E. Denoble ◽  
Kim M. Huffman ◽  
Thomas V. Stabler ◽  
Susan J. Kelly ◽  
Michael S. Hershfield ◽  
...  
Keyword(s):  
Uric Acid ◽  
Inflammasome Activation ◽  
Danger Signal ◽  
Increasing Risk

scholarly journals Inhibition of sterile danger signals, uric acid and ATP, prevents inflammasome activation and protects from alcoholic steatohepatitis in mice

2015 ◽  
Vol 63 (5) ◽  
pp. 1147-1155 ◽  
Author(s):  
Arvin Iracheta-Vellve ◽  
Jan Petrasek ◽  
Abhishek Satishchandran ◽  
Benedek Gyongyosi ◽  
Banishree Saha ◽  
...  
Keyword(s):  
Uric Acid ◽  
Inflammasome Activation ◽  
Danger Signals ◽  
Alcoholic Steatohepatitis

scholarly journals Danger signal uric acid is involved in ventilator-induced lung injury pathogenesis

Critical Care ◽  
2011 ◽  
Vol 15 (S1) ◽  
Author(s):  
M Kuipers ◽  
H Aslami ◽  
T Van der Poll ◽  
M Schultz ◽  
C Wieland
Keyword(s):  
Uric Acid ◽  
Lung Injury ◽  
Danger Signal ◽  
Ventilator Induced Lung Injury

scholarly journals Excess aldosterone is a critical danger signal for inflammasome activation in the development of renal fibrosis in mice

2015 ◽  
Vol 29 (9) ◽  
pp. 3899-3910 ◽  
Author(s):  
Hiroyuki Kadoya ◽  
Minoru Satoh ◽  
Tamaki Sasaki ◽  
Shun'ichiro Taniguchi ◽  
Masafumi Takahashi ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Inflammasome Activation ◽  
Danger Signal

scholarly journals Alum adjuvant boosts adaptive immunity by inducing uric acid and activating inflammatory dendritic cells

2008 ◽  
Vol 205 (4) ◽  
pp. 869-882 ◽  
Author(s):  
Mirjam Kool ◽  
Thomas Soullié ◽  
Menno van Nimwegen ◽  
Monique A.M. Willart ◽  
Femke Muskens ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Uric Acid ◽  
Lymph Node ◽  
Danger Signal ◽  
Th2 Response ◽  
Inflammatory Monocytes ◽  
Cellular And Humoral Immunity ◽  
Inflammatory Dendritic Cells ◽  
Deficient Mice

Alum (aluminum hydroxide) is the most widely used adjuvant in human vaccines, but the mechanism of its adjuvanticity remains unknown. In vitro studies showed no stimulatory effects on dendritic cells (DCs). In the absence of adjuvant, Ag was taken up by lymph node (LN)–resident DCs that acquired soluble Ag via afferent lymphatics, whereas after injection of alum, Ag was taken up, processed, and presented by inflammatory monocytes that migrated from the peritoneum, thus becoming inflammatory DCs that induced a persistent Th2 response. The enhancing effects of alum on both cellular and humoral immunity were completely abolished when CD11c+ monocytes and DCs were conditionally depleted during immunization. Mechanistically, DC-driven responses were abolished in MyD88-deficient mice and after uricase treatment, implying the induction of uric acid. These findings suggest that alum adjuvant is immunogenic by exploiting “nature's adjuvant,” the inflammatory DC through induction of the endogenous danger signal uric acid.

An Endogenous Danger Signal, Uric Acid, Attracts and Activates Human Eosinophils

2009 ◽  
Vol 123 (2) ◽  
pp. S252-S252
Author(s):  
T. Kobayashi ◽  
H. Kita
Keyword(s):  
Uric Acid ◽  
Danger Signal

Uric acid-mediated inflammasome activation in IL-6 primed innate immune cells is regulated by baricitinib

2020 ◽  
Vol 31 (1) ◽  
pp. 270-275 ◽  
Author(s):  
Jumpei Temmoku ◽  
Yuya Fujita ◽  
Naoki Matsuoka ◽  
Takeshi Urano ◽  
Makiko Yashiro Furuya ◽  
...  
Keyword(s):  
Uric Acid ◽  
Immune Cells ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells

Inflammasome activation by danger signals: extracellular ATP and pH

Inflammasome ◽  
2014 ◽  
Vol 1 (1) ◽  
Author(s):  
Takato Takenouchi ◽  
Mitsutoshi Tsukimoto ◽  
Makoto Hashimoto ◽  
Hiroshi Kitani
Keyword(s):  
P2x7 Receptor ◽  
Extracellular Atp ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Danger Signal ◽  
Interleukin 18 ◽  
Extracellular Acidification ◽  
Danger Signals ◽  
Acidic Extracellular Ph ◽  
Pro Inflammatory Cytokines

AbstractExtracellular ATP has been recognized as a danger signal that alerts the innate immune system. High extracellular concentrations of ATP can trigger the maturation and secretion of pro-inflammatory cytokines (e.g., interleukin-1β and interleukin-18) through the inflammasome-dependent activation of caspase-1. The P2X7 receptor, an ATP-gated cation channel, plays a pivotal role in ATP-induced NLRP3 inflammasome assembly. Recently, intriguing evidence has emerged that acidic extracellular pH acts as a danger signal that activates inflammasomes. Extracellular acidification frequently occurs at sites of inflammation, infection, or injury. In addition, large amounts of ATP are readily released into the extracellular space from damaged cells at such sites. Thus, it is assumed that the ATP/P2X7 receptor pathway regulates the inflammatory response under acidic extracellular conditions. Here, we briefly discuss the mutual effects of extracellular ATP and pH on inflammasome activation and consider their roles in the regulation of inflammation.

MPS 13-08 EXCESS ALDOSTERONE IS A CRITICAL DANGER SIGNAL FOR INFLAMMASOME ACTIVATION IN THE DEVELOPMENT OF RENAL FIBROSIS IN MICE

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e409-e410
Author(s):  
Minoru Satoh ◽  
Hiroyuki Kadoya ◽  
Tamaki Sasaki ◽  
Shun’ichiro Taniguchi ◽  
Masafumi Takahashi ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Inflammasome Activation ◽  
Danger Signal
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