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Published in: Inflammation Research 7/2011

01-07-2011 | Original Research Paper

Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice

Authors: Holly L. Rosenzweig, Jenna S. Clowers, Gabriel Nunez, James T. Rosenbaum, Michael P. Davey

Published in: Inflammation Research | Issue 7/2011

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Abstract

Objective

Activation of pattern recognition receptors (PRR) may contribute to arthritis. Here, we elucidated the role of NOD2, a genetic cause of inflammatory arthritis, and several other PRR in a murine model of inflammatory arthritis.

Methods

The roles of CR3, TLR2, MyD88, NOD1, NOD2, Dectin-1 and Dectin-2 were tested in vivo in arthritis elicited by intra-articular injections of zymosan, the fungal cell wall components curdlan, laminarin and mannan, and the bacterial cell wall peptidoglycan.

Results

Dectin-1, and to a lesser extent Dectin-2, contributed to arthritis. TLR2, MyD88 and CR3 played non-essential roles. Observations based on injection of curdlan, laminarin or mannan supported the dominant role of the Dectin-1 pathway in the joint. We demonstrated differential roles for NOD1 and NOD2 and identified NOD2 as a novel and essential mediator of zymosan-induced arthritis.

Conclusions

Together, Dectin-1 and NOD2 are critical, sentinel receptors in the arthritogenic effects of zymosan. Our data identify a novel role for NOD2 during inflammatory responses within joints.
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Metadata
Title
Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice
Authors
Holly L. Rosenzweig
Jenna S. Clowers
Gabriel Nunez
James T. Rosenbaum
Michael P. Davey
Publication date
01-07-2011
Publisher
SP Birkhäuser Verlag Basel
Published in
Inflammation Research / Issue 7/2011
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-011-0324-7

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