Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-7-19
pubmed:abstractText
Immune and inflammatory responses occurring in an injured nerve have been generally believed to contribute to the generation and maintenance of neuropathic pain. In this review, the authors demonstrate the upregulation of COX-2/prostaglandin E2, IL-6 and calcitonin gene-related peptide in invading macrophages and discuss possible mechanisms involved in their upregulation and how they contribute to the maintenance of neuropathic pain. By acting on nociceptors in dorsal root ganglion and local inflammatory cells via autocrine or paracrine pathways, these inflammatory mediators facilitate spontaneous ectopic activity and sustain nociceptive responses, an important mechanism underlying both ongoing and evoked neuropathic pain state. Targeting these mediators in injured nerve may provide novel therapeutic avenues to more successfully treat nerve injury-associated neuropathic pain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1744-7631
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
533-46
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Targeting invading macrophage-derived PGE2, IL-6 and calcitonin gene-related peptide in injured nerve to treat neuropathic pain.
pubmed:affiliation
Douglas Hospital Research Center, McGill University, Montréal, Quebec, H4H 1R3, Canada.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't