To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Systemic activation of To… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Contact form


Note! If you want an answer on a question you must specify your email address

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
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


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.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?

Denna text är utskriven från följande webbsida:
Utskriftsdatum: 2020-02-24