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

作者: Amin Mottahedin , Pernilla Svedin , Syam Nair , Carl-Johan Mohn , Xiaoyang Wang

DOI: 10.1177/0271678X17691292

关键词:

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

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