China University of Science and Technology to crack the mechanism of inflammation
August 14, 2017 Source: Technology Daily
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Chronic inflammatory reactions are involved in the development of almost all major human diseases, so understanding the process of inflammatory response may provide new strategies for disease treatment. In a recent issue of Nature Communication, a study reveals the important role of the intracellular chloride channel protein CLIC family in the activation of NLRP3 inflammatory bodies.
The research results are from the College of Life Sciences of China University of Science and Technology, the National Laboratory of Microscale and the Key Laboratory of Natural Immune and Chronic Diseases of the Chinese Academy of Sciences, Zhou Rongbin, Professor Jiang Wei, Research Group of Professor Wang Jun, Research Group of Professor Bai Li and Sun Yat-sen University. Professor Cui Wei's research team cooperated.
As a multi-protein complex, NLRP3 inflammatory bodies can promote the maturation and secretion of pro-inflammatory factors such as IL-1b and IL-18, thereby promoting the process of inflammatory response. In recent years, NLRP3 inflammatory bodies have been reported to be involved in the development of various major diseases such as type 2 diabetes, gout, and Parkinson, and to explore the activation mechanism of NLRP3 inflammatory bodies, which can provide potential therapeutic means.
NLRP3 inflammatory bodies can sense a variety of dangerous signals inside and outside the body, such as hyperglycemia, hyperlipidemia, uric acid crystals, cholesterol crystals, etc., but the molecular mechanism of the above-mentioned risk signals to induce NLRP3 activation is still unclear. Past research has shown that dangerous signals can induce the loss of intracellular potassium ions and mitochondrial damage, but the molecular mechanism of how intracellular potassium changes and mitochondrial damage induce subsequent assembly of inflammatory bodies has not been revealed.
The research found that the CLIC protein family can migrate to the cell membrane under the induction of reactive oxygen species induced by mitochondrial damage, mediating the outflow of intracellular chloride ions, thereby further promoting the assembly of NLRP3 inflammatory bodies and inhibiting the expression of CLIC family proteins. Or the activity can significantly inhibit the activation of NLRP3 inflammatory bodies. This work not only found that CLICs-mediated chloride efflux is a critical time upstream of NLRP3 inflammatory body assembly, but also suggests that MCCs can be targeted to alleviate NLRP3-related inflammatory diseases. (Reporter Wu Changfeng)
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