Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-4-27
pubmed:abstractText
Polymorphonuclear cells (PMN) are recruited in early inflammation and are believed to contribute to inflammatory pain. However, studies demonstrating a hyperalgesic role of PMN did not examine selective PMN recruitment or did not document effective PMN recruitment. We hypothesized that hyperalgesia does not develop after chemokine-induced PMN selective recruitment and is independent of PMN infiltration in complete Freund's adjuvant (CFA)-induced, local inflammation. PMN were recruited by intraplantar injection of CXC chemokine ligand 1 (CXCL1; keratinocyte-derived chemokine), CXCL2/3 (macrophage inflammatory protein-2), or CFA, with or without preceding systemic PMN depletion. Chemokine inoculation resulted in dose (0-30 microg)- and time (0-12 h)-dependent, selective recruitment of PMN as quantified by flow cytometry. CXCL2/3, but not CXCL1, was less effective at high doses, probably as a result of significant down-regulation of CXC chemokine receptor 2 expression on blood PMN. Neither chemokine caused mechanical or thermal hyperalgesia as determined by the Randall-Selitto and Hargreaves test, respectively, despite comparable expression of activation markers (i.e., CD11b, CD18, and L-selectin) on infiltrating PMN. In contrast, CFA injection induced hyperalgesia, independent of PMN recruitment. c-Fos mRNA and immunoreactivity in the spinal cord were increased significantly after inoculation of CFA-independent of PMN-migration but not of CXCL2/3. Measurement of potential hyperalgesic mediators showed that hyperalgesia correlated with local prostaglandin E2 (PGE2) but not with interleukin-1beta production. In summary, hyperalgesia, local PGE2 production, and spinal c-Fos expression occur after CFA-induced inflammation but not after CXCL1- or CXCL2/3-induced, selective PMN recruitment. Thus, PMN seem to be less important in inflammatory hyperalgesia than previously thought.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1022-32
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16522746-Animals, pubmed-meshheading:16522746-Antigens, Surface, pubmed-meshheading:16522746-Biological Markers, pubmed-meshheading:16522746-Chemokine CXCL1, pubmed-meshheading:16522746-Chemokine CXCL2, pubmed-meshheading:16522746-Chemokines, CXC, pubmed-meshheading:16522746-Chemotaxis, Leukocyte, pubmed-meshheading:16522746-Cytokines, pubmed-meshheading:16522746-Dinoprostone, pubmed-meshheading:16522746-Disease Models, Animal, pubmed-meshheading:16522746-Dose-Response Relationship, Drug, pubmed-meshheading:16522746-Down-Regulation, pubmed-meshheading:16522746-Freund's Adjuvant, pubmed-meshheading:16522746-Hyperalgesia, pubmed-meshheading:16522746-Inflammation, pubmed-meshheading:16522746-Male, pubmed-meshheading:16522746-Neutrophils, pubmed-meshheading:16522746-Pain, pubmed-meshheading:16522746-Pain Measurement, pubmed-meshheading:16522746-Posterior Horn Cells, pubmed-meshheading:16522746-Proto-Oncogene Proteins c-fos, pubmed-meshheading:16522746-Rats, pubmed-meshheading:16522746-Rats, Wistar, pubmed-meshheading:16522746-Time Factors, pubmed-meshheading:16522746-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Selective local PMN recruitment by CXCL1 or CXCL2/3 injection does not cause inflammatory pain.
pubmed:affiliation
Klinik für Anaesthesiologie und operative Intensivmedizin, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't