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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006100,
umls-concept:C0012472,
umls-concept:C0021755,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0224522,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C0871261,
umls-concept:C1283071,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1963578,
umls-concept:C2911692
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pubmed:issue |
2
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pubmed:dateCreated |
1989-7-31
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pubmed:abstractText |
Kinins are vasoactive peptides whose potent inflammatory and bone resorbing properties suggest a role for these autacoids in the pathogenesis of inflammatory arthritis. We used cultured human synovial cells as a model to evaluate the effects of bradykinin on articular tissue. In resting synovial cells, bradykinin was a relatively ineffective stimulus for PGE2 production. However, after a period of preincubation with the cytokine, IL-1, which is itself a stimulus for PGE2 production, synovial cells exhibited a further striking time- and dose-dependent response to bradykinin. Maximal release of PGE2 was observed in response to 10(-7) to 10(-6) M bradykinin after first pretreating the cells for 24 h with 5 to 10 U/ml of IL-1. rIL-1 alpha and IL-1 beta, as well as rTNF-alpha, induced a similar response to bradykinin in synovial cells, whereas recombinant IL-2 did not. The bradykinin analog, lysylbradykinin, was equipotent in inducing PGE2 release from IL-1 pretreated synovial cells, whereas des(Arg9) bradykinin, substance P, and neurokinins A and B were ineffective in this regard in both IL-1-pretreated and in resting cells. Synovial cells derived from patients with rheumatoid arthritis and osteoarthritis responded similarly to bradykinin. The synergistic response in PGE2 production induced by IL-1 and bradykinin was significantly inhibited by pretreatment with 1 microM indomethacin or dexamethasone (96 and 94% inhibition, respectively). In addition, the response was abrogated by pretreatment with 10 micrograms/ml of cycloheximide or actinomycin D (81 and 97% inhibition, respectively). These data provide the first description of synergism of IL-1 with a noncytokine peptide in human synovial cells. The ability of IL-1 to increase the responsiveness of synovial tissues to bradykinin may play an important role in potentiating inflammatory responses within the joint.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprost,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Neurokinin A,
http://linkedlifedata.com/resource/pubmed/chemical/Substance P
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
143
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
579-86
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2472445-Adjuvants, Immunologic,
pubmed-meshheading:2472445-Bradykinin,
pubmed-meshheading:2472445-Calcimycin,
pubmed-meshheading:2472445-Cells, Cultured,
pubmed-meshheading:2472445-Dinoprost,
pubmed-meshheading:2472445-Dinoprostone,
pubmed-meshheading:2472445-Humans,
pubmed-meshheading:2472445-Interleukin-1,
pubmed-meshheading:2472445-Kinetics,
pubmed-meshheading:2472445-Neurokinin A,
pubmed-meshheading:2472445-Substance P,
pubmed-meshheading:2472445-Synovial Membrane
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pubmed:year |
1989
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pubmed:articleTitle |
Preincubation of human synovial cells with IL-1 modulates prostaglandin E2 release in response to bradykinin.
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pubmed:affiliation |
Johns Hopkins University School of Medicine, Department of Medicine, Baltimore, MD.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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