title: TLR-4-dependent and -independent mechanisms of fetal brain injury in the setting of preterm birth.
abstract: In this study, we sought to assess how essential activation of toll-like receptor 4 (TLR-4) is to fetal brain injury from intrauterine inflammation. Both wild-type and TLR-4 mutant fetal central nervous system cells were exposed to inflammation using lipopolysaccharide in vivo or in vitro. Inflammation could not induce neuronal injury in the absence of glial cells, in either wild-type or TLR-4 mutant neurons. However, injured neurons could induce injury in other neurons regardless of TLR-4 competency. Our results indicate that initiation of neuronal injury is a TLR-4-dependent event, while propagation is a TLR-4-independent event.
authors: Maternal and Child Health Research Program, Department of OBGYN, Center for Research on Reproduction and Women's Health, University of Pennsylvania Health System, Philadelphia, PA 19104, USA. Kelsey.Breen@UCDenver.edu
authors: Kelsey
authors: K
authors: Breen
authors: Amy
authors: A
authors: Brown
authors: Irina
authors: I
authors: Burd
authors: Jinghua
authors: J
authors: Chai
authors: Alexander
authors: A
authors: Friedman
authors: Michal A
authors: MA
authors: Elovitz
mesh_terms: D000818:Animals; D001927:Brain Diseases / Q000196:embryology* / Q000209:etiology / Q000473:pathology; D004716:Endometritis / Q000150:complications; D005260:Female; D007249:Inflammation / Q000150:complications; D008070:Lipopolysaccharides / Q000008:administration & dosage; D051379:Mice; D008809:Mice, Inbred C3H; D008817:Mice, Mutant Strains; D009154:Mutation; D009474:Neurons / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D011247:Pregnancy; D047928:Premature Birth / Q000209:etiology; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000502:physiology*
chemical_list: D008070:Lipopolysaccharides; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4