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

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

Research output: Contribution to journalArticle

15 Scopus citations

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 nonessential 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.

Original languageEnglish (US)
Pages (from-to)705-714
Number of pages10
JournalInflammation Research
Volume60
Issue number7
DOIs
StatePublished - Jul 2011

Keywords

  • Arthritis models
  • In vivo inflammation
  • Innate immunity
  • NOD2
  • Zymosan

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

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