Differential Regulation of Endothelial Cell Permeability by High and Low Doses of Oxidized 1-Palmitoyl-2-Arachidonyl-<i>sn</i>-Glycero-3-Phosphocholine

Starosta, Vitaliy; Wu, Tianding; Zimman, Alejandro; Pham, Donald; Tian, Xinxin; Oskolkova, Olga; Bochkov, Valery N.; Berliner, Judith A.; Birukova, Anna A.; Birukov, Konstantin G.

doi:10.1165/rcmb.2011-0153oc

Cited by 55 publications

(60 citation statements)

References 52 publications

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“…Interestingly, in OxPAPC-treated neutrophils stimulated with opsonized S. aureus, a significant increase in the amount of ROS was seen. Previous studies reported that OxPAPC has the potential to increase ROS release in endothelial cells via activating the NADPH oxidase (58,59). Moreover, Fc gamma receptor (Fc␥R) signaling is known to trigger ROS release (60).…”

Section: Figmentioning

confidence: 99%

Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria

et al. 2017

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Oral bacteria are the main trigger for the development of periodontitis, and some species are known to modulate neutrophil function. This study aimed to explore the release of neutrophil extracellular traps (NETs), associated antimicrobial proteins, and reactive oxygen species (ROS) in response to periodontal bacteria, as well as the underlying pathways. Isolated peripheral blood neutrophils were stimulated with 19 periodontal bacteria. NET and ROS release, as well as the expression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured using fluorescence-based assays. NET and ROS release was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll-like receptors (TLRs). Moreover, bacterial entrapment by NETs was visualized microscopically, and bacterial killing was assessed by bacterial culture. Certain microorganisms, e.g., Veillonella parvula and Streptococcus gordonii, stimulated higher levels of ROS and NET release than others. NETs were found to entrap, but not kill, all periodontal bacteria tested. NADPH oxidase pathway modulators decreased ROS production but not NET production in response to the bacteria. Interestingly, TLR inhibitors did not impact ROS and NET release. These data suggest that the variability in the neutrophil response toward different bacteria may contribute to the pathogenesis of periodontal diseases by mechanisms such as bacterial avoidance of host responses and activation of neutrophils. Moreover, our results indicate that bacterium-stimulated NET release may arise in part via NADPH oxidase-independent mechanisms. The role of TLR signaling in bacterium-induced ROS and NET release needs to be further elucidated.KEYWORDS neutrophils, NETs, reactive oxygen species, periodontitis, oral bacteria P eriodontitis is initiated by the accumulation of microbial biofilms at and below the gingival margin. Indeed, it has been estimated that ϳ700 oral bacterial species and ϳ1,200 predominant phylotypes exist (1-3). Of these bacterial species, 5 major bacterial complexes (red, orange, yellow, green, and purple) have been identified by Socransky et al. using DNA probes (4) and are referred to here as Socransky complexes. The clustering and ordination analysis allowed them to assign microbial species to a color complex on the basis of the strength of the association with each other and the clinical staging of periodontitis. The biofilms which develop during disease are orchestrated to maximize their adherence, communication, and survival. The accumulation of bacterial species within the biofilm enables its development and perseverance, and certain bacteria, such as Fusobacterium nucleatum, are key orchestrators of biofilm formation and maturation (5).In susceptible individuals, dysbiosis and an aberrant host-microbe equilibrium can result in the onset of disease (6), where the microbial biofilm thrives by exploiting the

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Section: Figmentioning

confidence: 99%

Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria

et al. 2017

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“…It has been reported that Ox-PL can interact with ECs, monocyte/macrophages, platelets and SMCs through acting on different receptors to stimulate various signaling pathways underlying AS [157]. High concentration of Ox-PLs can disrupt endothelial integrity and increase endothelial permeability [158]. Ox-PLs can also facilitate macrophage lipid accumulation and foam cell formation by upregulating CD36 expression [159].…”

Section: The Pro-atherogenic Effect Of Fasmentioning

confidence: 99%

Lipoprotein lipase: From gene to atherosclerosis

Zhang

et al. 2014

Atherosclerosis

101

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“…However, even in HAEC, PEIPC at low concentrations decreases breakdown of the endothelial barrier (increased breakdown is seen in inflammation); whereas at higher concentrations PEIPC stimulates barrier breakdown. 25 In dendritic cells PEIPC strongly inhibits the pro-inflammatory action of bacterial lipids. 26, 27 While the effect of PEIPC is more complex, the effect of EI is mainly anti-inflammatory in both HAEC and dendritic cells.…”

Section: Discussionmentioning

confidence: 99%

An Epoxyisoprostane Is a Major Regulator of Endothelial Cell Function

Zhong¹,

Springstead²,

Al-Mubarak

et al. 2013

J. Med. Chem.

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The goal of these studies was to determine the effect of 5,6-epoxyisoprostane, EI, on human aortic endothelial cells (HAEC). EI can form as a phospholipase product of 1-palmitoyl-2-(5,6-epoxyisoprostane E2)-sn-glycero-3-phosphocholine, PEIPC, a pro-inflammatory molecule that accumulates in sites of inflammation where phospholipases are also increased. To determine the effect of EI on HAEC, we synthesized several stereoisomers of EI using a convergent approach from the individual optically pure building blocks, the epoxyaldehydes 5 and 6 and the bromoenones 14 and 16. The desired stereoisomer of EI can be prepared from these materials in only six operations and thus large amounts of the product can be obtained. The trans/trans isomers had the most potent activity, suggesting specificity in the interaction of EI with the cell surface. EI has potent anti-inflammatory effects in HAEC. EI strongly inhibits the production of MCP-1, a major monocyte chemotactic factor, and either decreases or minimally increases the levels of ten pro-inflammatory molecules increased by PEIPC. EI also strongly downregulates the inflammatory effects of IL-1β, a major inflammatory cytokine. Thus EI, a hydrolytic product of PEIPC, has potent anti-inflammatory function.

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Differential Regulation of Endothelial Cell Permeability by High and Low Doses of Oxidized 1-Palmitoyl-2-Arachidonyl-sn-Glycero-3-Phosphocholine

Cited by 55 publications

References 52 publications

Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria

Modulation of Neutrophil Extracellular Trap and Reactive Oxygen Species Release by Periodontal Bacteria

Lipoprotein lipase: From gene to atherosclerosis

An Epoxyisoprostane Is a Major Regulator of Endothelial Cell Function

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