Modulation of Adhesion Molecule Expression on Endothelial Cells after Induction by Lipopolysaccharide‐Stimulated Whole Blood

Nooteboom, A; Linden, C. J. Van Der; Hendriks, T.

doi:10.1111/j.0300-9475.2004.01413.x

Cited by 24 publications

(15 citation statements)

References 33 publications

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“…This is in line with previous studies demonstrating that plasma from E. coli-activated heparin anticoagulated whole blood (27) or conditioned medium with LPSactivated THP-1 cells, a monocytic cell line (28), caused ∼100-fold more potent activation of EC than did activating EC directly with the same concentration of E. coli or LPS. Thus, it seems that although E. coli can directly activate EC, this does not play a significant role due to the shear scale of leukocyte-induced activation.…”

Section: Discussionsupporting

confidence: 92%

Human Endothelial Cell Activation by Escherichia coli and Staphylococcus aureus Is Mediated by TNF and IL-1β Secondarily to Activation of C5 and CD14 in Whole Blood

Nymo

Gustavsen

Nilsson

et al. 2016

The Journal of Immunology

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Endothelial cells (EC) play a central role in inflammation. E-selectin and ICAM-1 expression are essential for leukocyte recruitment and are good markers of EC activation. Most studies of EC activation are done in vitro using isolated mediators. The aim of the present study was to examine the relative importance of pattern recognition systems and downstream mediators in bacteria-induced EC activation in a physiological relevant human model, using EC incubated with whole blood. HUVEC were incubated with human whole blood. Escherichia coli– and Staphylococcus aureus–induced EC activation was measured by E-selectin and ICAM-1 expression using flow cytometry. The mAb 18D11 was used to neutralize CD14, and the lipid A analog eritoran was used to block TLR4/MD2. C5 cleavage was inhibited using eculizumab, and C5aR1 was blocked by an antagonist. Infliximab and canakinumab were used to neutralize TNF and IL-1β. The EC were minimally activated when bacteria were incubated in serum, whereas a substantial EC activation was seen when the bacteria were incubated in whole blood. E. coli–induced activation was largely CD14-dependent, whereas S. aureus mainly caused a C5aR1-mediated response. Combined CD14 and C5 inhibition reduced E-selectin and ICAM-1 expression by 96 and 98% for E. coli and by 70 and 75% for S. aureus. Finally, the EC activation by both bacteria was completely abolished by combined inhibition of TNF and IL-1β. E. coli and S. aureus activated EC in a CD14- and C5-dependent manner with subsequent leukocyte secretion of TNF and IL-1β mediating the effect.

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Section: Discussionsupporting

confidence: 92%

Human Endothelial Cell Activation by Escherichia coli and Staphylococcus aureus Is Mediated by TNF and IL-1β Secondarily to Activation of C5 and CD14 in Whole Blood

Nymo

Gustavsen

Nilsson

et al. 2016

The Journal of Immunology

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“…The present study identified that the expression of IL-8 was continuously high along with the severity of lung injury, and peaked following injection of LPS for 4 h. The results also indicated that increased IL-8 expression may promote the migration of a large number of PMNs from the peripheral blood to the lung tissue, and PMNs release toxic substances, such as MPO. In addition, IL-8 may activate PMNs and directly damage the lung tissue cells (27). …”

Section: Discussionmentioning

confidence: 99%

Regulatory mechanism of pyrrolidine dithiocarbamate is mediated by nuclear factor-κB and inhibits neutrophil accumulation in ARDS mice

Wang

Zhao

et al. 2014

Experimental and Therapeutic Medicine

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The aim of the present study was to investigate the regulatory mechanism of nuclear factor (NF)-κB on polymorphonuclear neutrophil (PMN) accumulation and the inflammatory response in lung tissues with acute respiratory distress syndrome (ARDS), as well as the therapeutic effect of pyrrolidine dithiocarbamate (PDTC). Mouse models of ARDS were established by intraperitoneal injection of lipopolysaccharide (LPS). BALB/c mice were divided into control, LPS and PDTC + LPS groups. The expression of PMN adhesion molecules, CD11b/CD18 and intercellular adhesion molecule-1 (ICAM-1), were detected by immunohistochemistry, while the protein expression levels of NF-κB p65 in the lung tissue were analyzed by western blot analysis. In addition, flow cytometry was used to investigate the apoptosis rate of PMNs in the bronchoalveolar fluid, and the expression levels of interleukin (IL)-1β, IL-8 and tumor necrosis factor (TNF)-α and myeloperoxidase (MPO) activity were also determined. Following an intraperitoneal injection of LPS, alveolar septum rupture, pulmonary interstitial hyperemia and PMN infiltration in the alveolar was observed. The protein expression of p65 in the pulmonary cytoplasm decreased, while the expression of p65 in the nucleus increased. The levels of IL-8, IL-1β and TNF-α increased and the high expression status was maintained for 24 h. As the time increased, CD11b/CD18 and ICAM-1 expression increased, as well as MPO activity, while the apoptosis of PMNs was delayed. Compared with the LPS group, the expression of p65 in the pulmonary cytoplasm and the PMN apoptosis rate increased following PDTC intervention, while the expression of p65 in the nucleus decreased, as well as the expression levels of the cytokines and MPO activity. Therefore, PDTC reduced the production of inflammatory cytokines via the NF-κB pathway, which reduced the activation of PMNs in the lung tissue and promoted PMN apoptosis.

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“…Plasma of the same donors was used throughout the experiments. Our previous study demonstrated that the response of HUVEC to plasma obtained from these donors was essentially similar [14].…”

Section: Methodsmentioning

confidence: 99%

Modulation of endothelial monolayer permeability induced by plasma obtained from lipopolysaccharide-stimulated whole blood

Nooteboom

Bleichrodt

Hendriks

2006

Clinical and Experimental Immunology

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SummaryThe aim of this study was to elucidate the time course of the permeability response of endothelial monolayers after exposure to plasma obtained from lipopolysaccharide (LPS)-treated human whole blood; to investigate the role of apoptosis in monolayer permeability, and to inhibit the permeability increase, particularly after addition of the plasma stimulus. Human umbilical vein endothelial cells (HUVEC) were cultured on semiporous membranes and the permeability for albumin was measured after exposure, according to different schedules, to LPS-conditioned plasma. Apoptotic HUVEC were measured by both flow cytometry and ELISA. A variety of agents, including antibodies against cytokines, inhibitors of NF-κ κ κ κ B, and a caspase inhibitor, were added to HUVEC, either prior to or after the stimulus. A maximum increase of the permeability was achieved after 4-6 h of exposure to LPSconditioned plasma. This response was not accompanied by an increase in the number of apoptotic HUVEC. Administration of antibodies against both Tumour Necrosis Factor-α α α α (TNF-α α α α ) and Interleukin-1 β β β β (IL-1 β β β β ) to HUVEC within 1 h after stimulation significantly reduced the permeability increase. Similarly, pyrollidine di-thiocarbamate (PDTC), but not N-acetylcysteine, could prevent the permeability response, and was still effective when added within 2 h after LPS-conditioned plasma. The TNF-α α α α /IL-1 β β β β signal present in LPS-conditioned plasma appears to increase endothelial permeability through intracellular pathways that very likely involve the activation of NF-κ κ κ κ B. Although poststimulatory inhibition of the permeability response proves to be possible with agents such as PDTC, the window of opportunity appears very small if placed in a clinical perspective.

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Modulation of Adhesion Molecule Expression on Endothelial Cells after Induction by Lipopolysaccharide‐Stimulated Whole Blood

Cited by 24 publications

References 33 publications

Human Endothelial Cell Activation by Escherichia coli and Staphylococcus aureus Is Mediated by TNF and IL-1β Secondarily to Activation of C5 and CD14 in Whole Blood

Human Endothelial Cell Activation by Escherichia coli and Staphylococcus aureus Is Mediated by TNF and IL-1β Secondarily to Activation of C5 and CD14 in Whole Blood

Regulatory mechanism of pyrrolidine dithiocarbamate is mediated by nuclear factor-κB and inhibits neutrophil accumulation in ARDS mice

Modulation of endothelial monolayer permeability induced by plasma obtained from lipopolysaccharide-stimulated whole blood

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