Interleukin-1 and Tumor Necrosis Factor Activities Partially Account for Calvarial Bone Resorption Induced by Local Injection of Lipopolysaccharide

Chiang, Cheng‐Yang; Kyritsis, George; Graves, Dana T.; Amar, Salomon

doi:10.1128/iai.67.8.4231-4236.1999

Cited by 168 publications

(103 citation statements)

References 47 publications

(42 reference statements)

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“…These findings were correlated with data demonstrating that P. gingivalis LPS induces bone resorption via the CD14 receptor since murine antibodies directed against the LPS receptor blocking the osteolytic properties of LPS (25). Study showed that bone resorption induced by P. gingivalis LPS is accounted for by an increase in the number of osteoclasts and the area of bone resorption in IL-1 receptor and TNF receptor-deficient mice (38). Taken together, the data suggest that the effect of P. gingivalis LPS on bone resorption is mainly enhanced by osteoclatogenesis via the CD14 receptor.…”

Section: Discussionsupporting

confidence: 79%

Effects of CD14 receptors on tissue reactions induced by local injection of two gram‐negative bacterial lipopolysaccharides

Chiang

Shen

et al. 2003

J of Periodontal Research

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Lipopolysaccharide (LPS) was recognized by CD14, which may be an important mediator in the deleterious effects of LPS on the periodontal destruction. To investigate the roles of CD14 molecules on LPS-induced soft tissue inflammation and bone destruction, the tissues of CD14-deficient mice were examined histopathologically following a local injection of either Salmonella minnesota or Porphyromonas gingivalis LPS. In the first group, 12 mice received a local injection of 500 microg of purified P. gingivalis LPS and six mice were injected with saline to the calvaria as controls. In the second group 13 mice were injected subcutaneously on the laterally abdominal skin with 50 microg of S. minnesota LPS and three mice were injected with PBS. Mice were sacrificed at day 5. After histological preparation, the tissue sections of calvaria and soft tissue specimen were stained with tartrate-resistant acid phosphatase (TRAP) marker for osteoclast and macrophage. The soft tissue sections were also stained with hematoxylin & eosin (H&E). Resorption surface and osteoclast index were measured to quantify bone resorption. Necrotic area and inflammatory cell numbers were estimated to assess the situation of local inflammation. Our results indicated that LPS-induced bone resorption is inhibited in CD14-deficient mice. An increase in the number of total inflammatory cells was noticed in both CD14-deficient mice and wild-type mice; however, the cell numbers were less in CD14-deficient mice than those in wild-type mice (two- to three-fold decrease). Therefore, we conclude that the LPS-stimulated bone resorption is mainly via CD14 receptor but the LPS-induced soft tissue inflammation appears to be partially dependent on the receptor.

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Section: Discussionsupporting

confidence: 79%

Effects of CD14 receptors on tissue reactions induced by local injection of two gram‐negative bacterial lipopolysaccharides

Chiang

Shen

et al. 2003

J of Periodontal Research

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“…Synergistic stimulation of osteoclast differentiation by these cytokines may have important implications for a number of physiological and/or pathological conditions. Multiple cytokines appear to be involved in normal bone remodeling (26,44,64) as well as in stimulation of bone resorption in many pathological conditions including estrogen deficiency (27,38), hyperparathyroidism/humoral hypercalcemia of malignancy (23,24,61), hyperthyroidism (46), tumorinduced osteolysis (2,7,12,58), rheumatoid arthritis (19), lipopolysaccharide-induced osteolysis (1,11), and orthopedic implant loosening (36). Our CIMC-4 cells provide a model of osteoclast differentiation that should be Fig.…”

Section: Discussionmentioning

confidence: 99%

Cytokines synergistically induce osteoclast differentiation: support by immortalized or normal calvarial cells

Ragab¹,

Nalepka²,

Bi³

et al. 2002

American Journal of Physiology-Cell Physiology

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Conditionally immortalized murine calvarial (CIMC) cells that support differentiation of precursors into mature osteoclasts were isolated. All six CIMC cell lines supported osteoclast differentiation in response to 1,25-dihydroxyvitamin D(3) or interleukin (IL)-11. CIMC-4 cells also supported osteoclast differentiation in response to tumor necrosis factor (TNF)-alpha, IL-1beta, or IL-6. The resultant multinucleated cells expressed tartrate-resistant acid phosphatase and formed resorption lacunae on mineralized surfaces. CIMC-4 cells, therefore, establish an osteoclast differentiation assay that is responsive to many cytokines and does not rely on isolation of primary stromal support cells. Low concentrations of the cytokines synergistically stimulated differentiation when osteoclast precursors were cocultured with either CIMC-4 cells or primary calvarial cells. Osteoclast differentiation induced by all stimuli other than TNF-alpha was completely blocked by osteoprotegerin, whether the stimulators were examined alone or in combination. Moreover, study of precursors that lack TNF-alpha receptors showed that TNF-alpha induces osteoclast differentiation primarily through direct actions on osteoclast precursors, which is a distinct mechanism from that used by the other bone-resorptive agents examined in this study.

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“…The affinity of LPS to its pattern recognition receptors, such as the TLRs and CD14, enables discrimination between commensal and pathogenic species. The P. gingivalis LPS is a stimulator of proinflammatory responses and bone resorption, as demonstrated in experimental animal models (Chiang et al, 1999;Nishida et al, 2001). In vitro, it stimulates proinflammatory cytokine production of, for example, IL-1a, IL-1b, IL-6, IL-8, IL-18 and tumour necrosis factor (TNF)-a in monocytes (Zhou et al, 2005;Bostanci et al, 2007a, b;Hamedi et al, 2009).…”

Section: The Lps Of P Gingivalismentioning

confidence: 99%

Porphyromonas gingivalis: an invasive and evasive opportunistic oral pathogen

Bostancı

Belibasakis

2012

FEMS Microbiol Lett

462

413

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Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis, an inflammatory disease that destroys the tissues supporting the tooth, eventually leading to tooth loss. Porphyromonas gingivalis has can locally invade periodontal tissues and evade the host defence mechanisms. In doing so, it utilizes a panel of virulence factors that cause deregulation of the innate immune and inflammatory responses. The present review discusses the invasive and evasive strategies of P. gingivalis and the role of its major virulence factors in these, namely lipopolysaccharide, capsule, gingipains and fimbriae. Moreover, the role of P. gingivalis as a 'keystone' biofilm species in orchestrating a host response, is highlighted.

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Interleukin-1 and Tumor Necrosis Factor Activities Partially Account for Calvarial Bone Resorption Induced by Local Injection of Lipopolysaccharide

Cited by 168 publications

References 47 publications

Effects of CD14 receptors on tissue reactions induced by local injection of two gram‐negative bacterial lipopolysaccharides

Effects of CD14 receptors on tissue reactions induced by local injection of two gram‐negative bacterial lipopolysaccharides

Cytokines synergistically induce osteoclast differentiation: support by immortalized or normal calvarial cells

Porphyromonas gingivalis: an invasive and evasive opportunistic oral pathogen

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