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Infection and inflammation are known risk factors for neonatal brain injury. Mycoplasma and Gram-positive bacteria, for which Toll-like receptor 2 (TLR2) plays a key role in recognition and inflammatory response, are among the most common pathogens in the perinatal period. Here, we report that systemic activation of TLR2 by Pam3CSK4 (P3C) increases neural tissue loss and demyelination induced by subsequent hypoxia-ischemia (HI) in neonatal mice. High-resolution respirometry of brain isolated mitochondria revealed that P3C suppresses ADP-induced oxidative phosphorylation, the main pathway of cellular energy production. The results suggest that infection and inflammation might contribute to HI-induced energy failure.

Original publication

DOI

10.1177/0271678X17691292

Type

Journal article

Journal

J Cereb Blood Flow Metab

Publication Date

04/2017

Volume

37

Pages

1192 - 1198

Keywords

Cerebral palsy, birth asphyxia, metabolism, perinatal brain injury, Animals, Animals, Newborn, Brain, Female, Hypoxia-Ischemia, Brain, Ligands, Lipopeptides, Male, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Oxygen, Toll-Like Receptor 2