Acetate attenuates inflammasome activation through GPR43-mediated Ca2+-dependent NLRP3 ubiquitination

• Main Authors: Mengda Xu, Zhengyu Jiang, Changli Wang, Na Li, Lulong Bo, Yanping Zha, Jinjun Bian, Yan Zhang, Xiaoming Deng
• Format: Article
• Language: English
• Published: Nature Publishing Group 2019-07-01
• Series: Experimental and Molecular Medicine
• Online Access: https://doi.org/10.1038/s12276-019-0276-5

Inflammatory diseases: Putting on the brakes Acetate, a short-chain fatty acid, reduces activation of the NLRP3 inflammasome, a multiprotein complex that mediates inflammation. Acetate is produced by gut bacteria and can stimulate the synthesis of fat. High levels of acetate have been associated with diabetes, heart failure and tumor growth, but its effects on the immune system are largely unknown. A study led by Xiaoming Deng and Yan Zhang at the Second Military Medical University in Shanghai, China, shows that acetate has protective effects in mouse models of peritoneal and systemic inflammation and does not cause significant toxicity. Acetate suppresses inflammation by triggering a signaling pathway that reduces the activity of the NLRP3 inflammasome and leads to its degradation. These findings highlight a potential new approach for treating inflammatory diseases.