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Systemic activation of Toll-like receptor 2 suppresses mitochondrial respiration and exacerbates hypoxic-ischemic injury in the developing brain

Journal article
Authors Amin Mottahedin
Pernilla Svedin
Syam Nair
Carl-Johan Mohn
Xiaoyang Wang
Henrik Hagberg
C. Joakim Ek
Carina Mallard
Published in Journal of Cerebral Blood Flow and Metabolism
Volume 37
Issue 4
Pages 1192-1198
ISSN 0271-678X
Publication year 2017
Published at Institute of Neuroscience and Physiology
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 1192-1198
Language en
Links doi.org/10.1177/0271678x17691292
Keywords Cerebral palsy, birth asphyxia, metabolism, perinatal brain injury, cerebral ischemia/reperfusion injury, neonatal brain, inflammation, infection, infants, tlr2, sensitization, increases, responses, glutamate, Endocrinology & Metabolism, Hematology, Neurosciences & Neurology
Subject categories Obstetrics, Gynecology and Reproductive Medicine, Pediatrics

Abstract

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.

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