Effects of <i><scp>E</scp>nterococcus faecalis</i> lipoteichoic acid on receptor activator of nuclear factor‐κ<scp>B</scp> ligand and osteoprotegerin expression in periodontal ligament fibroblasts

Zhao, Liyan; Chen, J.; Cheng, Laiyang; Wang, X.; Du, Jie; Wang, F.; Zhang, Peng

doi:10.1111/iej.12127

Cited by 19 publications

(12 citation statements)

References 44 publications

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“…This has been demonstrated by studies showing that activation of TLR9 with CpG-DNA inhibits LPS-mediated TLR4 signaling in enterocytes and such inhibition involves a mechanism that depends on the inhibitory molecule IRAK-M (30). Interestingly, recent studies have demonstrated that IRAK inhibition significantly reduces LTA-stimulated increases in RANKL production in periodontal ligament fibroblasts (31). It remains to be determined whether the TLR9-derived RANKL production inhibition in B cells observed in our study is IRAK-dependent.…”

Section: Discussionsupporting

confidence: 62%

Activation of Toll‐like receptor 9 inhibits lipopolysaccharide‐induced receptor activator of nuclear factor kappa‐ B ligand expression in rat B lymphocytes

Yu¹,

Lin

Yu³

et al. 2014

Microbiology and Immunology

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B lymphocytes express multiple TLRs that regulate their cytokine production. We investigated the effect of TLR4 and TLR9 activation on receptor activator of NF-kB ligand (RANKL) expression by rat spleen B cells. Splenocytes or purified spleen B cells from Rowett rats were cultured with TLR4 ligand Escherichia coli LPS and/or TLR9 ligand CpG-oligodeoxynucleotide (CpG-ODN) for 2 days. RANKL mRNA expression and the percentage of RANKL-positive B cells were increased in rat splenocytes challenged by E. coli LPS alone. The increases were less pronounced when cells were treated with both CpG-ODN and E. coli LPS. Microarray analysis showed that expressions of multiple cyclin-dependent kinase (CDK) pathway-related genes were up-regulated only in cells treated with both E. coli LPS and CpG-ODN. This study suggests that CpG-ODN inhibits LPS-induced RANKL expression in rat B cells via regulation of the CDK pathway.Key words B lymphocytes, immune response, RANK ligand, Toll-like receptor.Not only in immune defense against microbial insults, but also in bone pathogenesis, immune responses to gramnegative bacterial infections, including periodontitis, involve activated B lymphocytes (1-3). Our studies and those of others have demonstrated that B lymphocytes produce RANKL in bone resorptive lesions of periodontal disease (3-5), and the excess RANKL shifts the balance of bone metabolism towards catabolism, resulting in pathological bone resorption (6). In order to design interventional strategies targeting amelioration of bone resorption in such situations, it is essential to clarify the mechanism(s) of control of B-cell-associated bone pathogenesis. While TLR signaling pathways play an important role in regulating B cell functions (7,8), including cytokine production, phagocytosis, and apoptosis (9), little is known about TLR signaling in the control of B cell-mediated bone pathogenesis.Although RANKL up-regulation is usually considered to be induced by pro-inflammatory cytokines, LPS from gram-negative bacteria can also directly increase amounts of RANKL mRNA in osteoblast-and osteoclast-lineage cells (10,11). Studies have demonstrated that activation of TLR2 or TLR4 results in RANKL-dependent osteoclastogenesis in rheumatoid arthritis synovium (12, 13). In addition, upon TLR9 ligation CpG-ODN reportedly induces osteoblast osteoclastogenic activity (14). However, other studies have shown that activation of TLRs (specifically TLR4 and TLR9) in early osteoclast precursors results in inhibition of RANKL-induced osteoclast differentiation via IL-12 (15). In human osteoclast precursor cell culture models, TLR ligands inhibit RANK expression by down-regulating cell surface expression of macrophage colony-stimulating factor receptor c-Fms, thereby List of Abbreviations: 7-AAD, 7-amino-actinomycin D; CDK, cyclin-dependent kinase; CDKI, cyclin-dependent kinase inhibitor; CpG-ODN, CpGoligodeoxynucleotide; EGFR, epidermal growth factor receptor; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; NF-kB, nuclear factor kappalight-ch...

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Section: Discussionsupporting

confidence: 62%

Activation of Toll‐like receptor 9 inhibits lipopolysaccharide‐induced receptor activator of nuclear factor kappa‐ B ligand expression in rat B lymphocytes

Yu¹,

Lin

Yu³

et al. 2014

Microbiology and Immunology

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“…They stimulate leukocytes, monocytes, and macrophages to release inflammatory mediators. 55 Thus, LTA may be associated with resistance to medications used during endodontic treatment, 56,57 also playing an important role in biofilm formation, providing bacterial resistance to antibiotics or disinfectants. It contributes to the virulence of E. faecalis by facilitating aggregation substance formation and plasmid transfer.…”

Section: Bacterial Virulence Factorsmentioning

confidence: 99%

Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology

2018

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Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.

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“…The equilibrium between OPG and RANKL activity has an essential role in the homeostasis of bone metabolism. In the pathological process of periodontal disease, the OPG/RANKL equilibrium is disrupted, leading to increased bone resorption ( 2 , 3 ). Human periodontal ligament fibroblasts (HPDLFs) are the primary cell type in the periodontal ligament and they contribute to the integrity of the periodontium.…”

Section: Introductionmentioning

confidence: 99%

Effects of IL-10 and glucose on expression of OPG and RANKL in human periodontal ligament fibroblasts

Zhang

Ding

Rao

et al. 2016

Braz J Med Biol Res

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The effects of interleukin-10 (IL-10) and glucose on mRNA and protein expression of osteoprotegerin (OPG), and its ligand, receptor activator of nuclear factor-κB ligand (RANKL), were investigated in human periodontal ligament fibroblasts (HPDLFs). Primary HPDLFs were treated with different concentrations of IL-10 (0, 1, 10, 25, 50, and 100 ng/mL) or glucose (0, 5.5, 10, 20, 30, and 40 mmol/L). Changes in mRNA and protein expression were examined using the reverse-transcription polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. After IL-10 treatment, mRNA and protein levels of OPG were increased, while mRNA and protein levels of RANKL were decreased (P<0.05), both in a concentration-dependent manner. Glucose stimulation had the opposite concentration-dependent effect to that of IL-10 on OPG and RANKL expression. IL-10 upregulated OPG expression and downregulated RANKL expression, whereas high glucose upregulated RANKL and downregulated OPG in HDPLFs. Abnormal levels of IL-10 and glucose may contribute to the pathogenesis of periodontal disease.

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Effects of Enterococcus faecalis lipoteichoic acid on receptor activator of nuclear factor‐κB ligand and osteoprotegerin expression in periodontal ligament fibroblasts

Cited by 19 publications

References 44 publications

Activation of Toll‐like receptor 9 inhibits lipopolysaccharide‐induced receptor activator of nuclear factor kappa‐ B ligand expression in rat B lymphocytes

Activation of Toll‐like receptor 9 inhibits lipopolysaccharide‐induced receptor activator of nuclear factor kappa‐ B ligand expression in rat B lymphocytes

Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology

Effects of IL-10 and glucose on expression of OPG and RANKL in human periodontal ligament fibroblasts

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