| Painful stimulation suppresses joint inflammation by inducing shedding of L-selectin from neutrophils. | |
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MedLine Citation:
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PMID: 10470085 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Although the inflammatory response is essential for protecting tissues from injury and infection, unrestrained inflammation can cause chronic inflammatory diseases such as arthritis, colitis and asthma. Physiological mechanisms that downregulate inflammation are poorly understood. Potent control might be achieved by regulating early stages in the inflammatory response, such as accumulation of neutrophils at the site of injury, where these cells release chemical mediators that promote inflammatory processes including plasma extravasation, bacteriocide and proteolysis. To access an inflammatory site, neutrophils must first adhere to the vascular endothelium in a process mediated in part by the leukocyte adhesion molecule L-selectin. This adhesion is prevented when L-selectin is shed from the neutrophil membrane. Although shedding of L-selectin is recognized as a potentially important mechanism for regulating neutrophils, its physiological function has not been demonstrated. Shedding of L-selectin may mediate endogenous downregulation of inflammation by limiting neutrophil accumulation at inflammatory sites. Here we show that activation of nociceptive neurons induces shedding of L-selectin from circulating neutrophils in vivo and that this shedding suppresses an ongoing inflammatory response by inhibiting neutrophil accumulation. These findings indicate a previously unknown mechanism for endogenous feedback control of inflammation. Failure of this mechanism could contribute to the etiology of chronic inflammatory disease. |
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Authors:
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H J Strausbaugh; P G Green; E Lo; K Tangemann; D B Reichling; S D Rosen; J D Levine |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Nature medicine Volume: 5 ISSN: 1078-8956 ISO Abbreviation: Nat. Med. Publication Date: 1999 Sep |
Date Detail:
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Created Date: 1999-09-24 Completed Date: 1999-09-24 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 9502015 Medline TA: Nat Med Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1057-61 Citation Subset: IM |
Affiliation:
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NIH Pain Center, UCSF, 521 Parnassus Avenue, San Francisco, California 94143-0440, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arthritis / blood, pathology, physiopathology* Bradykinin / antagonists & inhibitors, pharmacology Cells, Cultured Down-Regulation Electric Stimulation Feedback Flow Cytometry Hindlimb Hydroxamic Acids* L-Selectin / metabolism* Male Neurons, Afferent / physiology Neutrophils / metabolism*, physiology Nociceptors / physiology Pain / blood, physiopathology* Protease Inhibitors / pharmacology Rats Rats, Sprague-Dawley |
| Grant Support | |
ID/Acronym/Agency:
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AM32624/AM/NIADDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hydroxamic Acids; 0/Protease Inhibitors; 0/Ro 31-9790; 126880-86-2/L-Selectin; 58-82-2/Bradykinin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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