Authors: Yuan Tang, Fariborz Soroush, Shuang Sun, Elisabetta Liverani, Jordan C. Langston, Qingliang Yang, Laurie E. Kilpatrick, and Mohammad F. Kiani
Source: ncbi.nlm.nih.gov
Tang et al. Journal of Neuroinflammation (2018) 15:309
Received: July 9, 2018. Accepted: Oct 22, 2018. Published online: Nov 6, 2018
Synopsis: Neuroinflammation often develops in sepsis leading to activation of cerebral endothelium, increased permeability of the blood-brain barrier (BBB), and neutrophil infiltration. We have identified protein kinase C-delta (PKCδ) as a critical regulator of the inflammatory response and demonstrated that pharmacologic inhibition of PKCδ by a peptide inhibitor (PKCδ-i) protected endothelial cells, decreased sepsis-mediated neutrophil influx into the lung, and prevented tissue damage. The objective of this study was to elucidate the regulation and relative contribution of PKCδ in the control of individual steps in neuroinflammation during sepsis.