Linked Life Data

18003835

Source:http://linkedlifedata.com/resource/pubmed/id/18003835

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
46
pubmed:dateCreated
2007-11-16
pubmed:abstractText
Toll-like receptors (TLRs) bind specific components conserved among microorganisms as well as endogenous ligands produced by necrotic cells, injured axons, and the extracellular matrix. Here, we investigated whether TLRs are involved in regulating the immune response, Wallerian degeneration (WD), and nerve regeneration after sciatic nerve lesion. Early expression of interleukin-1beta and monocyte chemoattractant protein-1 was compromised in the sciatic nerve distal stump of mice deficient in TLR signaling. In addition, significantly fewer macrophages were recruited and/or activated in the sciatic nerve distal stump of TLR2-, TLR4-, and MyD88-deficient mice compared with wild-type littermates, whereas WD, axonal regeneration, and recovery of locomotor function were impaired. In contrast, animals that received a single microinjection of TLR2 and TLR4 ligands at the site of sciatic nerve lesion had faster clearance of the degenerating myelin and recovered earlier than saline-injected control rats. Finally, rats that had altered innate immune response through dexamethasone treatment exhibited three times more myelin debris in their sciatic nerve distal stump and a significant delay in recovery of locomotor function. Our results provide strong evidence that TLR signaling plays a critical role in orchestrating the innate immune response leading to efficient and rapid clearance of inhibitory myelin debris and nerve regeneration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
12565-76
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18003835-Animals, pubmed-meshheading:18003835-Chemokine CCL2, pubmed-meshheading:18003835-Chemotaxis, Leukocyte, pubmed-meshheading:18003835-Immunity, Innate, pubmed-meshheading:18003835-Interleukin-1beta, pubmed-meshheading:18003835-Macrophages, pubmed-meshheading:18003835-Mice, pubmed-meshheading:18003835-Mice, Inbred C57BL, pubmed-meshheading:18003835-Mice, Knockout, pubmed-meshheading:18003835-Myelin Sheath, pubmed-meshheading:18003835-Nerve Fibers, Myelinated, pubmed-meshheading:18003835-Nerve Regeneration, pubmed-meshheading:18003835-Peripheral Nerve Injuries, pubmed-meshheading:18003835-Peripheral Nerves, pubmed-meshheading:18003835-Phagocytosis, pubmed-meshheading:18003835-Rats, pubmed-meshheading:18003835-Recovery of Function, pubmed-meshheading:18003835-Sciatic Neuropathy, pubmed-meshheading:18003835-Signal Transduction, pubmed-meshheading:18003835-Toll-Like Receptor 2, pubmed-meshheading:18003835-Toll-Like Receptor 4, pubmed-meshheading:18003835-Toll-Like Receptors, pubmed-meshheading:18003835-Wallerian Degeneration
pubmed:year
2007
pubmed:articleTitle
Toll-like receptor signaling is critical for Wallerian degeneration and functional recovery after peripheral nerve injury.
pubmed:affiliation
Laboratory of Molecular Endocrinology, CHUL Research Center, and Department of Anatomy and Physiology, Faculty of Medicine, Laval University, Ste-Foy, Québec, Canada G1V 4G2.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't