EPIGALLOCATECHIN GALLATE INHIBITS EXPRESSION OF RECEPTOR ACTIVATOR OF NF-.KAPPA.B LIGAND IN MOUSE OSTEOBLAST INFECTED WITH STAPHYLOCOCCUS AUREUS

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Osteomyelitis is a generally severe infection characterized by inflammatory destruction of the bone. This disease is often refractory and subject to recurrence.Staphylococcus aureus, the Gram-positive organism, is the most common causative agent of osteomyelitis. In bone marrow inflammation caused by the infection withS. aureus, the production of various cytokines is induced. Inflammatory cytokines such as IL-1, IL-6, and TNF-a and receptor activator of NF-κ B ligand (RANKL) are candidate cytokines which are produced by osteoblasts and promote bone resorption. Epigallocatechin gallate (EGCg), the main constituent of tea catechins, exhibits antibacterial, antioxidative, and anti-inflammatory activities. Here, we examined the inhibitory effect of EGCg on production of IL-1α, IL-1β, IL-6, TNF-α, and RANKL in mouse osteoblst infected withS. aureus. Normal osteoblastes produced IL-1α, IL-6, and RANKL but not IL-1β and TNF-α after exposure toS. aureus. In contrast, pretreatment with EGCg to osteoblasts significantly inhibited the production of IL-1α, IL-6, and RANKL. These results indicate that the reduction of IL-1α, IL-6 and RANKL in osteoblasts by EGCg may result in the prevention and therapy for inflammatory bone diseases.