Sphingosine-1-phosphate receptor 2 (S1PR2) deficiency decreased macrophage pyroptosis and improved survival in E. coli sepsis. These beneficial effects were attributed to the decreased caspase-11 activation of S1PR2-deficient macrophages. S1PR2 and caspase-11 may be promising new targets for treatment of sepsis. In an in vivo mouse model of Gram-negative sepsis, deletion of the gene for sphingosine-1-phosphate receptor 2 (S1PR2) reduced pyroptosis, possibly by decreased activation of caspase-11, and increased survival. S1PR2 and caspase-11 may be testable targets in sepsis.

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