Scholz Holger, Eder Claudia
Charité - Universitätsmedizin Berlin, Institute of Physiology, 10117 Berlin, Germany.
Charité - Universitätsmedizin Berlin, Institute of Physiology, 10117 Berlin, Germany.
J Neuroimmunol. 2017 Sep 15;310:107-110. doi: 10.1016/j.jneuroim.2017.07.004. Epub 2017 Jul 10.
Inflammasomes regulate microglial caspase-1 activation and subsequent neuroinflammatory processes in brain pathology. In the present study, we have identified inflammasomes causing caspase-1 activation following stimulation of microglia with lysophosphatidylcholine (LPC), a proinflammatory lipid generated under pathological conditions in the brain. LPC-induced caspase-1 activation in microglia was found to depend on LPS prestimulation, inflammasome NLRP3 and adaptor molecule ASC. Furthermore, knockdown of inflammasome NLRC4 inhibited LPC-stimulated caspase-1 activity in microglia, suggesting the requirement of two inflammasomes for optimal caspase-1 activity.
炎性小体在脑病理学中调节小胶质细胞半胱天冬酶-1的激活及随后的神经炎症过程。在本研究中,我们鉴定出在用溶血磷脂酰胆碱(LPC)刺激小胶质细胞后可导致半胱天冬酶-1激活的炎性小体,LPC是大脑病理条件下产生的一种促炎脂质。发现LPC诱导的小胶质细胞半胱天冬酶-1激活依赖于脂多糖预刺激、炎性小体NLRP3和接头分子ASC。此外,炎性小体NLRC4的敲低抑制了LPC刺激的小胶质细胞半胱天冬酶-1活性,提示需要两种炎性小体来实现最佳的半胱天冬酶-1活性。