albicans may also be through recognition of glucan by the dectin 1 TLR2 receptor complex. Dectin 1, a major glucan receptor, has a number of antimi crobial functions in phagocytes including induction of cytokines and chemokines, possibly by collaborating with TLRs, involvement in endocytosis and phagocytosis and pro duction of the respiratory burst. Rat dectin 1 is involved in immune responses against fungi. Laminarin, a soluble form of glucan blocks signaling through dectin 1. Lami narin decreases TNF production by macrophages in response to zymosan and C. albicans infection. In the cur rent study laminarin partially blocked the increase in COX 2 mRNA that is seen when synovial fibroblasts are infected with C. albicans. This indicates that signaling through dectin 1 has a partial role in the upregulation of COX 2 gene expression.
This may be through direct contact between C. albicans and synovial fibroblasts EMD 121974 as the elevation of COX 2 gene expression was similar in trans well experiments and experiments with laminarin where contact between C. albicans and synovial fibroblasts was possible. Conclusions We show for the first time that COX 2 induction and PGE2 production occurs following infection of C. albicans to syno vial fibroblasts and that this requires ERK12 activation and is associated with NFB activation. These interactions may sig nificantly contribute to the detrimental inflammatorycatabolic activities of synovial fibroblasts in septic arthritis induced by C. albicans and other fungi. Competing interests The authors declare that they have no competing interests.
Authors contributions HSL conceived of the study, participated in its design and coordination, participated in the interpretation of results, and predominantly inhibitor Masitinib drafted the manuscript. CSL supervised the experiments by CJY. CJY carried out the RT PCR, western blotting, EMSA, immunocytochemistry, and ELISA. SLS per formed the statistical analysis. DMS helped to discuss the results and draft the manuscript. All authors read and approved the final manuscript. Introduction Chondrocytes maintain articular cartilage through coordinated production and degradation of the extracellular matrix. Type II collagen, aggrecan, and link proteinencoded by the genes Col2a1, Agc1 and Hapln1, respectivelyare major compo nents of the articular cartilage extracellular matrix. Type II collagen is the major structural collagen of articular cartilage. Aggrecan is the most abundant proteoglycan, and is responsible for resisting the compressive forces imposed on articulating joints. Finally, link protein stabilizes the associ ation of aggrecan with hyaluronic acid. The expression of these ECM proteins is regulated by transcription factors within the nucleus promoting or inhibiting transcript production.