Expression analysis of genes related to the Toll-like receptor signaling in osteoarthritic chondrocytes

Abstract

Osteoarthritis (OA) is known as a degenerative disease of articular cartilage, but accumulating evidence implies that inflammation has a critical role in OA pathogenesis. Unlike rheumatoid arthritis (RA), OA is characterized by low-grade inflammation, which is caused by a chronic innate immune system. The activation of innate immune receptors such as Toll-like receptors (TLRs) causes inflammatory and catabolic signaling in chondrocytes. TLRs are the most well-known receptors of pattern recognition receptors (PRRs) that detect microbial components termed damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). Accessory molecules are essential for the activation of TLRs and are required for biosynthesis and signal transfer of TLRs. Among TLR family members, TLR2 and TLR4 have been reported that TLR2 or TLR4 activation modulates expression of pro-inflammatory cytokines and MMPs, which are a catabolic enzyme of an extracellular matrix. However, the mechanistic basis for TLR signaling-related molecules, such as TLRs and accessory molecules, accompanying the low-grade inflammation in OA pathogenesis is still questionable. We found that expression of TLR signaling-related molecules elevated in osteoarthritic chondrocyte. Thus, the present study provided a possible role of TLR signaling-related molecules as an important regulator of cartilage inflammatory responses in OA pathogenesis.