Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-10-15
pubmed:abstractText
Rheumatoid arthritis (RA) is a chronic autoimmune arthritis that affects approximately 1% of the population. Synovial inflammation cannot fully explain the level of pain reported by patients and facilitation of pain processing at the spinal level has been implicated. We characterized the K/BxN serum transfer arthritis model as a model of joint inflammation-induced pain and examined pharmacologic responsiveness and spinal glia activation. Mechanical allodynia developed congruently with joint swelling. Surprisingly, allodynia persisted after resolution of inflammation. At the peak of joint inflammation (days 4-10), hypersensitivity was attenuated with i.p. etanercept, gabapentin, and ketorolac. Following resolution of synovial inflammation (days 19-23), only gabapentin relieved allodynia. The superficial dorsal horn of arthritic mice displayed increased staining of microglia at early and late time points, but astrocyte staining increased only during the inflammatory phase. ATF3, a marker of nerve injury, was significantly increased in the lumbar dorsal root ganglia during the late phase (day 28). Hence, serum transfer in the K/BxN serum transfer arthritis model produces a persistent pain state, where the allodynia during the inflammatory state is attenuated by TNF and prostaglandin inhibitors, and the pharmacology and histochemistry data suggest a transition from an inflammatory state to a state that resembles a neuropathic condition over time. Therefore, the K/BxN serum transfer model represents a multifaceted model for studies exploring pain mechanisms in conditions of joint inflammation and may serve as a platform for exploring novel treatment strategies for pain in human arthritic conditions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1872-6623
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
394-403
pubmed:dateRevised
2011-11-1
pubmed:meshHeading
pubmed-meshheading:20739123-Activating Transcription Factor 3, pubmed-meshheading:20739123-Amines, pubmed-meshheading:20739123-Analgesics, pubmed-meshheading:20739123-Analysis of Variance, pubmed-meshheading:20739123-Animals, pubmed-meshheading:20739123-Arthritis, Rheumatoid, pubmed-meshheading:20739123-Astrocytes, pubmed-meshheading:20739123-Autoantibodies, pubmed-meshheading:20739123-Behavior, Animal, pubmed-meshheading:20739123-Cyclohexanecarboxylic Acids, pubmed-meshheading:20739123-Disease Models, Animal, pubmed-meshheading:20739123-Ganglia, Spinal, pubmed-meshheading:20739123-Glucose-6-Phosphate Isomerase, pubmed-meshheading:20739123-Knee Joint, pubmed-meshheading:20739123-Male, pubmed-meshheading:20739123-Mice, pubmed-meshheading:20739123-Mice, Inbred C57BL, pubmed-meshheading:20739123-Mice, Inbred NOD, pubmed-meshheading:20739123-Mice, Transgenic, pubmed-meshheading:20739123-Microglia, pubmed-meshheading:20739123-Pain, pubmed-meshheading:20739123-Pain Measurement, pubmed-meshheading:20739123-Pain Threshold, pubmed-meshheading:20739123-Physical Stimulation, pubmed-meshheading:20739123-Receptors, Antigen, T-Cell, pubmed-meshheading:20739123-Serum, pubmed-meshheading:20739123-Spinal Cord, pubmed-meshheading:20739123-Time Factors, pubmed-meshheading:20739123-gamma-Aminobutyric Acid
pubmed:year
2010
pubmed:articleTitle
Characterization of the acute and persistent pain state present in K/BxN serum transfer arthritis.
pubmed:affiliation
Department of Pharmacology, University of California, San Diego, La Jolla, CA, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural