Role of macrophages in LPS-induced osteoblast and PDL cell apoptosis

Thammasitboon, Kewalin; Goldring, Steven R.; Boch, Jason A.

doi:10.1016/j.bone.2005.10.013

Cited by 54 publications

(52 citation statements)

References 43 publications

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“…Macrophages have been shown to produce tissue injury in different organs, including bone, through the release of MMPs and proinflammatory cytokines (50). To analyze whether factors secreted by B. abortus-infected macrophages could induce osteoblast injury, we studied the effects of conditioned medium from infected macrophages on osteoblast cells.…”

Section: B Abortus Invades and Multiplies In Primary Mouse Osteoblasmentioning

confidence: 99%

“…TNF-␣ is a proinflammatory cytokine that induces apoptosis in a number of cell systems, including osteoblasts (21,50). To test the effect of TNF-␣ present in supernatants from B. abortus-infected macrophages on osteoblast apoptosis, we stimulated osteoblasts with supernatants from B. abortus-infected macrophages pretreated with a neutralizing anti-TNF-␣ antibody or an isotype control.…”

Section: B Abortus Invades and Multiplies In Primary Mouse Osteoblasmentioning

confidence: 99%

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Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

et al. 2012

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ABSTRACTOsteoarticular brucellosis is the most common presentation of the active disease in humans. Loss of bone is a serious complication of localized bacterial infection of bones or the adjacent tissue, and brucellosis proved not to be the exception. The skeleton is a dynamic organ system which is constantly remodeled. Osteoblasts are responsible for the deposition of bone matrix and are thought to facilitate the calcification and mineralization of the bone matrix, and their function could be altered under infectious conditions. In this article, we describe immune mechanisms wherebyBrucella abortusmay invade and replicate within osteoblasts, inducing apoptosis, inhibiting mineral and organic matrix deposition, and inducing upregulation of RANKL expression. Additionally, all of these mechanisms contributed in different ways to bone loss. These processes implicate the activation of signaling pathways (mitogen-activated protein kinases [MAPK] and caspases) involved in cytokine secretion, expression of activating molecules, and cell death of osteoblasts. In addition, considering the relevance of macrophages in intracellularBrucellasurvival and proinflammatory cytokine secretion in response to infection, we also investigated the role of these cells as modulators of osteoblast survival, differentiation, and function. We demonstrated that supernatants fromB. abortus-infected macrophages may also mediate osteoblast apoptosis and inhibit osteoblast function in a process that is dependent on the presence of tumor necrosis factor alpha (TNF-α). These results indicate thatB. abortusmay directly and indirectly harm osteoblast function, contributing to the bone and joint destruction observed in patients with osteoarticular complications of brucellosis.

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Section: B Abortus Invades and Multiplies In Primary Mouse Osteoblasmentioning

confidence: 99%

Section: B Abortus Invades and Multiplies In Primary Mouse Osteoblasmentioning

confidence: 99%

Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

et al. 2012

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“…Moreover, it plays a significant role in the control of proliferation, differentiation and apoptosis 10) . Regarding the cells found in periodontal tissues, TNF-α has been shown to trigger apoptosis in osteoblasts and PDL cells 11) .…”

Section: Introductionmentioning

confidence: 99%

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Funakoshi

Yamaguchi

Asano

et al. 2013

J. Hard Tissue Biology.

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The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygen species (ROS)-induced apoptosis in PDL cells. Following the application of orthodontic force to maxillary first molars, the molars were investigated using immunohistochemical analysis. The cell cycle and apoptosis were assessed in compression force-treated PDL cells using flow cytometry. Furthermore, we assayed the effect on ROS generation by DCFDA fluorescence. In vivo study revealed an increased number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. Taken together, these results provide new information on compression force-induced G1 arrest and apoptosis in hPDL cells.

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“…16,17 LPS is the leading stimulus that initiates the host response in the periodontal pocket and activates macrophages cells to release proinflammatory cytokines. [18][19][20][21] Consequently, this proinflammatory cytokine can lead to inflammatory cascades and result in periodontium destruction. So the extent of affected tissue in periodontitis is directly associated with the production of cytokines.…”

Section: Discussionmentioning

confidence: 99%

Minocycline hydrochloride nanoliposomes inhibit the production of TNF-α in LPS-stimulated macrophages

Liu¹,

Yang²

2012

IJN

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Background:As an adjunctive treatment of chronic periodontitis, it seems that the application of periocline or the other antimicrobials is effective against periodontopathogens. In this study, nanoliposomes were investigated as carriers of minocycline hydrochloride and the inhibition effects of minocycline hydrochloride nanoliposomes on the proliferation and lipopolysaccharide (LPS)-stimulated production of tumor necrosis factor-α (TNF-α) of macrophages were elucidated. Methods: After stimulation with 10 µg/mL LPS, murine macrophages (ANA-1) were treated with 10, 20, 40, 50 and 70 µg/mL 2% minocycline hydrochloride nanoliposomes, minocycline hydrochloride solution, and periocline for 6, 12, 24, 48 and 60 hours, respectively. A tetrazolium (MTT) assay was used to evaluate macrophages cell proliferation rate and the levels of TNF-α mRNA were measured by SYBR Green Real Time PCR. Results: Ten to 70 µg/mL 2% minocycline hydrochloride nanoliposomes, minocycline hydrochloride solution, and periocline showed dose-and time-dependent inhibition of ANA-1 proliferation. Minocycline hydrochloride nanoliposomes showed dose-and ratio-dependent inhibition of LPS-stimulated TNF-α secretion of ANA-1. The inhibition effect of 10 µg/mL minocycline hydrochloride nanoliposomes was significantly better than that of two positive control groups, and equated to that of 60 or 70 µg/mL periocline. The expression of TNF-α mRNA in experimental group continued to reduce linearly with time. Conclusion: All three preparations of minocycline hydrochloride showed dose-and timedependent inhibition of proliferation of ANA-1. Minocycline hydrochloride nanoliposomes have stronger and longer inhibition effect on LPS-stimulated TNF-α secretion of macrophages cell than minocycline hydrochloride solution and periocline.

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Role of macrophages in LPS-induced osteoblast and PDL cell apoptosis

Cited by 54 publications

References 43 publications

Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Minocycline hydrochloride nanoliposomes inhibit the production of TNF-α in LPS-stimulated macrophages

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Role of macrophages in LPS-induced osteoblast and PDL cell apoptosis

Cited by 54 publications

References 43 publications

Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

Brucella abortus Invasion of Osteoblasts Inhibits Bone Formation

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Minocycline hydrochloride nanoliposomes inhibit the production of TNF-&alpha; in LPS-stimulated macrophages

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Minocycline hydrochloride nanoliposomes inhibit the production of TNF-α in LPS-stimulated macrophages