Dendritic Cells, Antibodies Reactive with oxLDL, and Inflammation

Tew, John G.; Shikh, Mohey Eldin El; Sayed, Rania M. El; Schenkein, Harvey A.

doi:10.1177/0022034511407338

Cited by 26 publications

(25 citation statements)

References 63 publications

(116 reference statements)

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“…These cells activate an immune response, either acting as antigen-presenting cells or producing IL-12 and IL-18 that consequently promote interferon- γ (IFN- γ ) secretion by NK cells and later by T cells [16]. Periodontal ligament fibroblasts (PDLFs) and gingival fibroblasts (GF) are the main cells of periodontal soft connective tissue and are accessed as the microorganisms breach the epithelial barrier.…”

Section: Resident Cells and Innate Immunitymentioning

confidence: 99%

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Benedetto

Gigante

Colucci

et al. 2013

Clinical and Developmental Immunology

250

249

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Periodontal disease (PD), or periodontitis, is defined as a bacterially induced disease of the tooth-supporting (periodontal) tissues. It is characterized by inflammation and bone loss; therefore understanding how they are linked would help to address the most efficacious therapeutic approach. Bacterial infection is the primary etiology but is not sufficient to induce the disease initiation or progression. Indeed, bacteria-derived factors stimulate a local inflammatory reaction and activation of the innate immune system. The innate response involves the recognition of microbial components by host cells, and this event is mediated by toll-like receptors (TLRs) expressed by resident cells and leukocytes. Activation of these cells leads to the release of proinflammatory cytokines and recruitment of phagocytes and lymphocytes. Activation of T and B cells initiates the adaptive immunity with Th1 Th2 Th17 Treg response and antibodies production respectively. In this inflammatory scenario, cytokines involved in bone regulation and maintenance have considerable relevance because tissue destruction is believed to be the consequence of host inflammatory response to the bacterial challenge. In the present review, we summarize host factors including cell populations, cytokines, and mechanisms involved in the destruction of the supporting tissues of the tooth and discuss treatment perspectives based on this knowledge.

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Section: Resident Cells and Innate Immunitymentioning

confidence: 99%

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Benedetto

Gigante

Colucci

et al. 2013

Clinical and Developmental Immunology

250

249

View full text Add to dashboard Cite

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“…As a recent example, infection by Aggregatibacter actinomycetemcomitans or Chlamydophila pneumoniae or host response against them have been associated with coronary obstruction [27] and elevated levels of P. gingivalis and A. actinomycetemcomitans – specific serum IgG were associated with AS [28]. Specifically, the resident dendritic cell interaction with phosphorylcholine- and cardiolipin-specific IgG2 bound to microorganisms and with microbial products may enhance dendritic cell IL12 production, IFN-γ response, macrophage (Mϕ) activation, chronic inflammation and eventually, plaque destabilization [29]. …”

Section: Oral Diseases and Systemic Inflammationsmentioning

confidence: 99%

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

Kozarov

2011

Future Cardiol.

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To portray the chronic inflammation in atherosclerosis, leukocytic cell types involved in the immune response to invading pathogens are often the focus. However, atherogenesis is a complex pathological deterioration of the arterial walls, where vascular cell types are participants with regards to deterioration and disease. Since other recent reviews have detailed the role of both the innate and adaptive immune response in atherosclerosis, herein we will summarize the latest developments regarding the association of bacteria with vascular cell types: infections as a risk factor for atherosclerosis; bacterial invasion of vascular cell types; the atherogenic sequelae of bacterial presence such as endothelial activation and blood clotting; and the identification of the species that are able to colonize this niche. The evidence of a polybacterial infectious component of the atheromatous lesions opens the doors for exploration of the new field of vascular infectology and for the study of atherosclerosis microbiome.

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“…The oxidized low-density lipoprotein (oxLDL) is one of the most important risk factors for atherosclerosis (Zeibig et al, 2011;Tew et al, 2012). One of the earliest effects of atherosclerosis is endothelial cell dysfunction and inflammatory chemokine secretion to increase the number of mononuclear macrophages (Simionescu, 2007).…”

Section: Introductionmentioning

confidence: 99%

TLR4/NF-κB signaling pathway-mediated and oxLDL-induced up-regulation of LOX-1, MCP-1, and VCAM-1 expressions in human umbilical vein endothelial cells

Feng

Tang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to investigate the function and signaling pathway of Toll-like receptor 4 (TLR4) in oxidized lowdensity lipoprotein (oxLDL)-induced up-regulated expressions of oxidized LDL receptor 1 (LOX-1), monocyte chemoattractant protein 1 (MCP-1), and vascular cell adhesion molecule 1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs). HUVECs were incubated with different oxLDL concentrations (0, 20, 40, 60, and 80 µg/mL) for 24 and 48 h. The influence of oxLDL on TLR4, LOX-1, MCP- TLR4/NF-kB signaling pathway-mediated oxLDL 1, and VCAM-1 expressions in HUVECs was detected by real-time polymerase chain reaction and Western blot analysis. HUVECs were transfected with small interfering RNA targeting TLR4 (siTLR4), in which protein expressions of LOX-1, MCP-1, and VCAM-1, and the nuclear translocation of NF-kB (P50) were detected by Western blot. After 48 h of processing HUVECs with pyrrolidine dithiocarbamate (PDTC), protein expressions of TLR4, LOX-1, MCP-1, and VCAM-1 were detected by Western blot. OxLDL induced a concentrationdependent up-regulation of mRNA and protein expressions of TLR4, LOX-1, MCP-1, and VCAM-1 in HUVECs (P < 0.001). siTLR4 significantly reduced protein expressions of LOX-1, MCP-1, VCAM-1, and reduced the NF-kB (P50) nuclear translocation (P < 0.001). PDTC significantly inhibited protein expressions of TLR4, LOX-1, MCP-1, and VCAM-1 (P < 0.001). Results of this study demonstrate that the TLR4/NF-κB signaling pathway has an important function in the up-regulation of oxLDL-induced expressions of LOX-1, MCP-1, and VCAM-1 in HUVECs.

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Dendritic Cells, Antibodies Reactive with oxLDL, and Inflammation

Abstract: A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental.

Cited by 26 publications

References 63 publications

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Bacterial Invasion of Vascular Cell Types: Vascular Infectology and Atherogenesis

TLR4/NF-κB signaling pathway-mediated and oxLDL-induced up-regulation of LOX-1, MCP-1, and VCAM-1 expressions in human umbilical vein endothelial cells

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