Journal
INFLAMMATION RESEARCH
Volume 60, Issue 7, Pages 705-714Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-011-0324-7
Keywords
Arthritis models; NOD2; In vivo inflammation; Innate immunity; Zymosan
Categories
Funding
- US Department of Veterans Affairs
- National Eye Institute [EY019020]
- Gerlinger Award
- Stan and Madelle Rosenfeld Family Trust
- William C. Kuzell Foundation
- American College of Rheumatology and Research
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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. 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. 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. 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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