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Text
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URL Address
<a href="http://doi.org/10.1172/jci119506" target="_blank" rel="noreferrer">http://doi.org/10.1172/jci119506</a>
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Title
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Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats
Publisher
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The Journal Of Clinical Investigation
Date
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1997
Subject
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Humans; Male; Time Factors; Analysis of Variance; Animals; Regression Analysis; Rats; Biomarkers of Pain; RNA; Genetic; Biomarkers Reference List; Inflammation/physiopathology; Freund's Adjuvant; Hindlimb; Pain/immunology/physiopathology; Corticotropin-Releasing Hormone/pharmacology; Wistar; Messenger/biosynthesis; beta-Endorphin/biosynthesis; Interleukin-1/pharmacology; Lymph Nodes/metabolism; Pro-Opiomelanocortin/biosynthesis; T-Lymphocytes/drug effects/immunology/metabolism; Transcription
Creator
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Cabot PJ; Carter L; Gaiddon C; Zhang Q; Schafer M; Loeffler JP; Stein C
Description
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Localized inflammation of a rat's hindpaw elicits an accumulation of beta-endorphin-(END) containing immune cells. We investigated the production, release, and antinociceptive effects of lymphocyte-derived END in relation to cell trafficking. In normal animals, END and proopiomelanocortin mRNA were less abundant in circulating lymphocytes than in those residing in lymph nodes (LN), suggesting that a finite cell population produces END and homes to LN. Inflammation increased proopiomelanocortin mRNA in cells from noninflamed and inflamed LN. However, END content was increased only in inflamed paw tissue and noninflamed LN-immune cells. Accordingly, corticotropin-releasing factor and IL-1beta released significantly more END from noninflamed than from inflamed LN-immune cells. This secretion was receptor specific, calcium dependent, and mimicked by potassium, consistent with vesicular release. Finally, both agents, injected into the inflamed paw, induced analgesia which was blocked by the co-administration of antiserum against END. Together, these findings suggest that END-producing lymphocytes home to inflamed tissue where they secrete END to reduce pain. Afterwards they migrate to the regional LN, depleted of the peptide. Consistent with this notion, immunofluorescence studies of cell suspensions revealed that END is contained predominantly within memory-type T cells. Thus, the immune system is important for the control of inflammatory pain. This has implications for the understanding of pain in immunosuppressed conditions like cancer or AIDS.
1997
Identifier
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<a href="http://doi.org/10.1172/jci119506" target="_blank" rel="noreferrer">10.1172/jci119506</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
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Journal Article
1997
Analysis of Variance
Animals
Backlog
beta-Endorphin/biosynthesis
Biomarkers of Pain
Biomarkers Reference List
Cabot PJ
Carter L
Corticotropin-Releasing Hormone/pharmacology
Freund's Adjuvant
Gaiddon C
Genetic
Hindlimb
Humans
Inflammation/physiopathology
Interleukin-1/pharmacology
Journal Article
Loeffler JP
Lymph Nodes/metabolism
Male
Messenger/biosynthesis
Pain/immunology/physiopathology
Pro-Opiomelanocortin/biosynthesis
Rats
Regression Analysis
RNA
Schafer M
Stein C
T-Lymphocytes/drug effects/immunology/metabolism
The Journal Of Clinical Investigation
Time Factors
transcription
Wistar
Zhang Q