Liver X receptors agonists suppress NLRP3 inflammasome activation
| Autor: | Wei Chen, Feng-Hua Zhou, Chao-Ying Ma, Ning Li, Kun-Yu Li, Guiqiu Hu, Shuai Qi, Yongjun Yang, Chongtao Du, Shui-Xing Yu, Xiao-Zhu Hu, Qian-Qian Lei, Shi-Yuan Feng |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Agonist medicine.medical_specialty medicine.drug_class Inflammasomes Immunology Interleukin-1beta Inflammation Biology Peritonitis Biochemistry Cell Line 03 medical and health sciences Mice In vivo Internal medicine NLR Family Pyrin Domain-Containing 3 Protein medicine Immunology and Allergy Animals Liver X receptor Molecular Biology Liver X Receptors Caspase 3 Inflammasome Hematology Cell biology 030104 developmental biology Endocrinology NLRP3 inflammasome activation medicine.symptom medicine.drug Signal Transduction |
| Zdroj: | Cytokine. 91 |
| ISSN: | 1096-0023 |
| Popis: | Inflammasomes are multiprotein complexes that control the production of IL-1β and IL-18. NLRP3 inflammasome, the most characterized inflammasome, plays prominent roles in defense against infection, however aberrant activation is deleterious and leads to diseases. Therefore, its tight control offers therapeutic promise. Liver X receptors (LXRs) have significant anti-inflammatory properties. Whether LXRs regulate inflammasome remains unresolved. We thus tested the hypothesis that LXR's anti-inflammatory properties may result from its ability to suppress inflammasome activation. In this study, LXRs agonists inhibited the induction of IL-1β production, caspase-1 cleavage and ASC oligomerization by NLRP3 inflammasome. The agonists also inhibited inflammasome-associated mtROS production. Importantly, the agonists inhibited the priming of inflammasome activation. In vivo data also showed that LXRs agonist prevented NLRP3-dependent peritonitis. In conclusion, LXRs agonists are identified to potently suppress NLRP3 inflammasome and the regulation of LXRs signaling is a potential therapeutic for inflammasome-driven diseases. |
| Databáze: | OpenAIRE |
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