Nitric oxide production by a human osteoblast cell line stimulated with <i>Aggregatibacter actinomycetemcomitans</i> lipopolysaccharide

Sosroseno, Wihaskoro; Bird, P. S.; Seymour, G. J.

doi:10.1111/j.1399-302x.2008.00475.x

Cited by 20 publications

(17 citation statements)

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“…The presence of NO in periodontal disease may reflect the participation of an additional mediator of bone resorption responsible for disease progression (Batista et al 2002). Periodontitis involving alveolar bone destruction are mediated by bacterial products including endotoxin or lipopolysaccharide (LPS), which can directly induce cell death or apoptosis, and by stimulating NO production in macrophages, epithelial cells and fibroblasts (Albina et al 1993, Tiwari et al 2006, Sosroseno et al 2009). On the other hand, the generation of high levels of NO in various cells is associated with autocytotoxicity, suppression of carcinogenesis and inhibition of metastasis (Shimojo et al 1999, Kim et al 2008, Tewari et al 2008.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide induces apoptosis in human gingival fibroblast through mitochondria‐dependent pathway and JNK activation

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Nitric oxide induces apoptosis in human gingival fibroblast through mitochondria‐dependent pathway and JNK activation

et al. 2014

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“…LPS can directly induce cell death or apoptosis in many cell types, and by stimulating NO production in macrophages, epithelial cells, and fibroblasts [29-31]. The production of high levels of NO in various cells is associated with autocytotoxicity, suppression of carcinogenesis, and inhibition of metastasis that result partially from induction of apoptosis [32].…”

Section: Discussionmentioning

confidence: 99%

Synergic induction of human periodontal ligament fibroblast cell death by nitric oxide and N-methyl-D-aspartic acid receptor antagonist

Seo

Cha

Woo

et al. 2011

J Periodontal Implant Sci

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PurposeNitric oxide (NO) has been known as an important regulator of osteoblasts and periodontal ligament cell activity. This study was performed to investigate the relationship between NO-mediated cell death of human periodontal ligament fibroblasts (PDLFs) and N-methyl-D-aspartic acid (NMDA) receptor antagonist (+)-5-methyl-10, 11-dihydro-5H-dibenzo[a,d]cyclohepten-5, 10-imine hydrogen maleate (MK801).MethodsHuman PDLFs were treated with various concentrations (0 to 4 mM) of sodium nitroprusside (SNP) with or without 200 µM MK801 in culture media for 16 hours and the cell medium was then removed and replaced by fresh medium containing MTS reagent for cell proliferation assay. Western blot analysis was performed to investigate the effects of SNP on the expression of Bax, cytochrome c, and caspase-3 proteins. The differences for each value among the sample groups were compared using analysis of variance with 95% confidence intervals.ResultsIn the case of SNP treatment, as a NO donor, cell viability was significantly decreased in a concentration-dependent manner. In addition, a synergistic effect was shown when both SNP and NMDA receptor antagonist was added to the medium. SNP treated PDLFs exhibited a round shape in culture conditions and were dramatically reduced in cell number. SNP treatment also increased levels of apoptotic marker protein, such as Bax and cytochrome c, and reduced caspase-3 in PDLFs. Mitogen-activated protein kinase signaling was activated by treatment of SNP and NMDA receptor antagonist.ConclusionsThese results suggest that excessive production of NO may induce apoptosis and that NMDA receptor may modulate NO-induced apoptosis in PDLFs.

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“…These results indicated that CPA‐c mediated apoptosis of MC3T3‐E1 murine osteoblastic cells via the Fas system, independent of Bcl‐2 or NO synthase (Yamamoto et al ., ). In contrast to A. actinomycetemcomitans CPA‐c mechanisms driving apoptosis in osteoblasts, A. actinomycetemcomitans ‐derived LPS induced production of NO in the HOS human osteoblastic cell line (Sosroseno et al ., ), which suggests that LPS may contribute to A. actinomycetemcomitans proapoptotic actions on osteoblastic cells via NO signaling.…”

Section: Aggregatibacter Actinomycetemcomitans Osteoimmuno‐modulatorymentioning

confidence: 97%

Aggregatibacter actinomycetemcomitans, a potent immunoregulator of the periodontal host defense system and alveolar bone homeostasis

Herbert

Novince

Kirkwood

2015

Molecular Oral Microbiology

115

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Summary Aggregatibacter actinomycetemcomitans is a perio-pathogenic bacteria that has long been associated with localized aggressive periodontitis. The mechanisms of its pathogenicity have been studied in humans and pre-clinical experimental models. Although different serotypes of A. actinomycetemcomitans have differential virulence factor expression, A. actinomycetemcomitans cytolethal distending toxin (CDT), leukotoxin, and lipopolysaccharide (LPS) have been most extensively studied in the context of modulating the host immune response. Following colonization and attachment in the oral cavity, A. actinomycetemcomitans employs CDT, leukotoxin, and LPS to evade host innate defense mechanisms and drive a pathophysiologic inflammatory response. This supra-physiologic immune response state perturbs normal periodontal tissue remodeling/turnover and ultimately has catabolic effects on periodontal tissue homeostasis. In this review, we have divided the host response into two systems: non-hematopoietic and hematopoietic. Non-hematopoietic barriers include epithelium and fibroblasts that initiate the innate immune host response. The hematopoietic system contains lymphoid and myeloid-derived cell lineages that are responsible for expanding the immune response and driving the pathophysiologic inflammatory state in the local periodontal microenvironment. Effector systems and signaling transduction pathways activated and utilized in response to A. actinomycetemcomitans will be discussed to further delineate immune cell mechanisms during A. actinomycetemcomitans infection. Finally, we will discuss the osteo-immunomodulatory effects induced by A. actinomycetemcomitans and dissect the catabolic disruption of balanced osteoclast-osteoblast mediated bone remodeling, which subsequently leads to net alveolar bone loss.

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Nitric oxide production by a human osteoblast cell line stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide

Abstract: These results therefore suggest that A. actinomycetemcomitans lipopolysaccharide may induce the production of NO by HOS cells via a CD14-TLR4 molecule complex, a cAMP-PKA pathway, as well as by a PTK, PKC, PLA2, and lipoxygenase-dependent mechanism.

Cited by 20 publications

References 52 publications

Nitric oxide induces apoptosis in human gingival fibroblast through mitochondria‐dependent pathway and JNK activation

Nitric oxide induces apoptosis in human gingival fibroblast through mitochondria‐dependent pathway and JNK activation

Synergic induction of human periodontal ligament fibroblast cell death by nitric oxide and N-methyl-D-aspartic acid receptor antagonist

Aggregatibacter actinomycetemcomitans, a potent immunoregulator of the periodontal host defense system and alveolar bone homeostasis

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