Epigallocatechin gallate suppresses expression of receptor activator of NF-κB ligand (RANKL) in Staphylococcus aureus infection in osteoblast-like NRG cells

Ishida, Ikuo; Kohda, Chikara; Yanagawa, Yoko; Miyaoka, Hiroaki; Shimamura, Tadakatsu

doi:10.1099/jmm.0.47029-0

Cited by 24 publications

(13 citation statements)

References 37 publications

(27 reference statements)

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“…Bacterial pathogens can stimulate osteoclastogenesis, either directly or indirectly, which can potentiate bone resorption, leading to bone destruction (31,36 (19). Based on these findings, we undertook this study to evaluate the production of RANK-L from S. aureus-infected primary osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts

et al. 2008

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Osteomyelitis is an inflammatory disease of the bone that is characterized by the presence of necrotic bone tissue and increased osteoclast activity. Staphylococcus aureus is responsible for approximately 80% of all cases of human osteomyelitis. While the disease is especially difficult to treat, the pathogenesis of S. aureus-induced osteomyelitis is poorly understood. Elucidating the molecular mechanisms by which S. aureus induces osteomyelitis could lead to a better understanding of the disease and its progression and development of new treatments. Osteoblasts can produce several soluble factors that serve to modulate the activity or formation of osteoclasts. Receptor activator of NF-B ligand (RANK-L) and prostaglandin E 2 (PGE 2 ) are two such molecules which can promote osteoclastogenesis and stimulate bone resorption. In addition, previous studies in our laboratory have shown that osteoblasts produce inflammatory cytokines, such as interleukin 6, following infection with S. aureus, which could induce COX-2 and in turn PGE 2 , further modulating osteoclast recruitment and differentiation. Therefore, we hypothesized that following infection with S. aureus, osteoblasts will express increased levels of RANK-L and PGE 2 . The results presented in this study provide evidence for the first time that RANK-L mRNA and protein and PGE 2 expression are upregulated in S. aureus-infected primary osteoblasts. In addition, through the use of the specific COX-2 inhibitor NS 398, we show that when PGE 2 production is inhibited, RANK-L production is decreased. These data suggest a mechanism whereby osteoblasts regulate the production of RANK-L during infection.Osteomyelitis is a severe infection of bone tissue that results in progressive inflammatory destruction of bone (41). The gram-positive organism Staphylococcus aureus is the most common causative agent of osteomyelitis, accounting for approximately 80% of all human cases (27). It is often necessary that infected bone be debrided, tissues reconstructed, and longterm antibiotic therapy utilized (18). The current treatment for osteomyelitis is often traumatic and expensive and often leads to further selection of antibiotic-resistant strains of S. aureus. The growing incidence of antibiotic-resistant S. aureus strains can explain the recurrent attacks of osteomyelitis in patients undergoing therapy. In addition, the pathogenesis of S. aureusinduced osteomyelitis is poorly understood. Elucidating the mechanisms by which S. aureus induces osteomyelitis could therefore lead to a better understanding of the disease, its progression, and development of new treatments.Bone remodeling involves a continuous, coordinated equilibrium between bone synthesis and bone resorption, and two cell populations are responsible for the continual process (23). Osteoclasts drive the resorption of bone by acidification and release of lysosomal enzymes, while osteoblasts produce components of the bone matrix, principally type I collagen. Osteoblasts also produce factors which serve to modulate the ...

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts

et al. 2008

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“…), there are also some effects that may contribute to the total antimicrobial effect in infected individuals. These effects include inhibition of inflammation (particularly inflammation caused by oxidative stress, such as vascular), more specifically, by increasing the synthesis of nitric oxide (Yamakuchi et al, 2008), inhibiting angiotensin II and IL-6-induced C-reactive protein expression (Li et al, 2012), suppression of IL-6 and RANKL production in infected osteoblast-like cells (Ishida et al, 2007), inhibiting IL-8 production (Hirao et al, 2010), and inhibiting hyaluronidase activity (activated by chronic inflammation) by inhibition of IL-12 (Adcocks et al, 2002). …”

Section: Antimicrobial Properties Of Green Teamentioning

confidence: 99%

The antimicrobial possibilities of green tea

Reygaert¹

2014

Front. Microbiol.

270

186

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Green tea is a popular drink, especially in Asian countries, although its popularity continues to spread across the globe. The health benefits of green tea, derived from the leaves of the Camellia sinensis plant, have been studied for many years. Fairly recently, researchers have begun to look at the possibility of using green tea in antimicrobial therapy, and the potential prevention of infections. The particular properties of catechins found in the tea have shown promise for having antimicrobial effects. There are four main catechins (polyphenols) found in green tea: (-)-epicatechin (EC), (-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC), and (-)-epigallocatechin-3-gallate (EGCG). Three of these, ECG, EGC, and EGCG have been shown to have antimicrobial effects against a variety of organisms. These catechins have exhibited a variety of antimicrobial mechanisms. The results of studies on the antimicrobial effects of green tea have shown that the potential for preventive and therapeutic purposes is present. Further data collection on studies performed with human consumption during the course of infections, and studies on the occurrence of infections in populations that consume regular amounts of green tea will be necessary to complete the picture of its antimicrobial possibilities.

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“…Takai et al [160] found that EGCG significantly reduced the IL-6 synthesis and IL-6 mRNA expression induced by platelet-derived growth factor-BB through suppression of the SAPK/JNK pathway in osteoblast-like MC3T3-E1 cells. Moreover, Ishida [161] reported that EGCG controls inflammatory bone resorption in chronic osteomyelitis by inhibiting the production of IL-6 and RANKL in osteoblasts infected with S. aureus .…”

Section: Possible Mechanisms Of Green Tea On Osteo-protectionmentioning

confidence: 99%

Green tea and bone metabolism

et al. 2009

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Osteoporosis is a major health problem in both elderly women and men. Epidemiological evidence has shown an association between tea consumption and the prevention of age-related bone loss in elderly women and men. Ingestion of green tea and green tea bioactive compounds may be beneficial in mitigating bone loss of this population and decreasing their risk of osteoporotic fractures. This review describes the effect of green tea or its bioactive components on bone health, with an emphasis on: (i) the prevalence and etiology of osteoporosis, (ii) the role of oxidative stress and antioxidants in osteoporosis, (iii) green tea composition and bioavailability, (iv) the effects of green tea and its active components on osteogenesis, osteoblastogenesis, and osteoclastogenesis from human epidemiological, animal, as well as cell culture studies, (v) possible mechanisms explaining the osteoprotective effects of green tea bioactive compounds, (vi) other bioactive components in tea that benefit bone health, and (vii) a summary and future direction of green tea and bone health research and the translational aspects. In general, tea and its bioactive components might decrease the risk of fracture by improving bone mineral density (BMD) and supporting osteoblastic activities while suppressing osteoclastic activities.

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Epigallocatechin gallate suppresses expression of receptor activator of NF-κB ligand (RANKL) in Staphylococcus aureus infection in osteoblast-like NRG cells

Cited by 24 publications

References 37 publications

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts

The antimicrobial possibilities of green tea

Green tea and bone metabolism

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Epigallocatechin gallate suppresses expression of receptor activator of NF-κB ligand (RANKL) in Staphylococcus aureus infection in osteoblast-like NRG cells

Cited by 24 publications

References 37 publications

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E2in Infected Murine Osteoblasts

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E2in Infected Murine Osteoblasts

The antimicrobial possibilities of green tea

Green tea and bone metabolism

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Product

Resources

About

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts

Staphylococcus aureusInduces Expression of Receptor Activator of NF-κB Ligand and Prostaglandin E₂in Infected Murine Osteoblasts