RGD Reference Report - Interactions between bradykinin (BK) and cell adhesion molecule (CAM) expression in peptidoglycan-polysaccharide (PG-PS)-induced arthritis. - Rat Genome Database

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Interactions between bradykinin (BK) and cell adhesion molecule (CAM) expression in peptidoglycan-polysaccharide (PG-PS)-induced arthritis.

Authors: Sainz, IM  Uknis, AB  Isordia-Salas, I  DeLa Cadena, RA  Pixley, RA  Colman, RW 
Citation: Sainz IM, etal., FASEB J. 2004 May;18(7):887-9. Epub 2004 Mar 4.
RGD ID: 1625760
Pubmed: PMID:15001555   (View Abstract at PubMed)
DOI: DOI:10.1096/fj.03-0835fje   (Journal Full-text)

Bradykinin (BK), a vasoactive, proinflammatory nonapeptide, promotes cell adhesion molecule (CAM) expression, leukocyte sequestration, inter-endothelial gap formation, and protein extravasation in postcapillary venules. These effects are mediated by bradykinin-1 (B1R) and-2 (B2R) receptors. We delineated some of the mechanisms by which BK could influence chronic inflammation by altering CAM expression on leukocytes, endothelium, and synovium in joint sections of peptidoglycan-polysaccharide-injected Lewis rats. Blocking B1R results in significantly increased joint inflammation. Immunohistochemistry of the B1R antagonist group revealed increased leukocyte and synovial CD11b and CD54 expression and increased CD11b and CD44 endothelial expression. B2R antagonism decreased leukocyte and synovial CD44 and CD54 and endothelial CD11b expression. Although these findings implicate B2R involvement in the acute phase of inflammation by facilitating leukocyte activation (CD11b), homing (CD44), and transmigration (CD54). Treatment with a B2R antagonist did not affect the disease evolution in this model. In contrast, when both BK receptors are blocked, the aggravation of inflammation by B1R blockade is neutralized and there is no difference from the disease-untreated model. Our findings suggest that B1R and B2R signaling show physiologic antagonism. B1R signaling suggests involvement in down-regulation of leukocyte activation, transmigration, and homing. Further studies are needed to evaluate the B1 receptor agonist's role in this model.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Arthritis  ISOBdkrb1 (Rattus norvegicus)1625760; 1625760 RGD 
Experimental Arthritis  IMP 1625760 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bdkrb1  (bradykinin receptor B1)

Genes (Mus musculus)
Bdkrb1  (bradykinin receptor, beta 1)

Genes (Homo sapiens)
BDKRB1  (bradykinin receptor B1)


Additional Information