Cyclooxygenase metabolites mediate glomerular monocyte chemoattractant protein-1 formation and monocyte recruitment in experimental glomerulonephritis1 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-02

AUTHORS

A Schneider, S Harendza, G Zahner, T Jocks, U Wenzel, G Wolf, F Thaiss, U Helmchen, R A Stahl

ABSTRACT

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) has been shown to play a significant role in the recruitment of monocytes/macrophages in experimental glomerulonephritis. Whereas a number of inflammatory mediators have been characterized that are involved in the expression of MCP-1 in renal disease, little is known about repressors of chemokine formation in vivo. We hypothesized that cyclooxygenase (COX) products influence the formation of MCP-1 and affect inflammatory cell recruitment in glomerulonephritis. METHODS: The effect of COX inhibitors was evaluated in the antithymocyte antibody model and an anti-glomerular basement membrane model of glomerulonephritis. Rats were treated with the COX-1/COX-2 inhibitor indomethacin and the selective COX-2 inhibitors meloxicam and SC 58125. Animals were studied at 1 hour, 24 hours, and 5 days after induction of the disease. RESULTS: Indomethacin, to a lesser degree the selective COX-2 inhibitors, enhanced glomerular MCP-1 and RANTES mRNA levels. Indomethacin enhanced glomerular monocyte chemoattractant activity an the infiltration of monocytes/macrophages at 24 hours and 5 days. CONCLUSIONS: Our studies demonstrate that COX products may serve as endogenous repressors of MCP-1 formation in experimental glomerulonephritis. The data suggest that COX-1 and COX-2 products mediate these effects differently because the selective COX-2 inhibitors had less influence on chemokine expression. More... »

PAGES

430-441

Identifiers

URI

http://scigraph.springernature.com/pub.10.1046/j.1523-1755.1999.00265.x

DOI

http://dx.doi.org/10.1046/j.1523-1755.1999.00265.x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025518553

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9987068


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