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Inflamm Res. 2011 Jul;60(7):705-14. doi: 10.1007/s00011-011-0324-7. Epub 2011 Mar 20.

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

Author information

1
Oregon Health and Science University, Mail stop: L467 AD, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA. rosenzwh@ohsu.edu

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.

PMID:
21424514
PMCID:
PMC3352590
DOI:
10.1007/s00011-011-0324-7
[Indexed for MEDLINE]
Free PMC Article

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