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

Amin Mottahedin, Pernilla Svedin, Syam Nair, Carl-Johan Mohn, Xiaoyang Wang, Henrik Hagberg, Joakim Ek, Carina Mallard

Research output: Contribution to journalArticlepeer-review

32 Citations (Scopus)
15 Downloads (Pure)

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.
Original languageEnglish
Article number28139935
Pages (from-to)1-7
Number of pages7
JournalJournal of Cerebral Blood Flow and Metabolism
Early online date31 Jan 2017
DOIs
Publication statusE-pub ahead of print - 31 Jan 2017

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