2018
DOI: 10.1016/j.jaci.2017.07.026
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Histamine and Toll-like receptor ligands synergistically induce endothelial cell gap formation by the extrinsic coagulating pathway

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Cited by 26 publications
(44 citation statements)
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“…where α 1 is the positive constant implying the histamine concentration where the inhibition effect is the highest, and α 2 is the positive constant determining the highest level of inhibition effect (Fig 2B Right). For the inhibitory regulation, we assume that there exists a self-inhibition mechanism which is directly regulated in a histamine concentration-dependent manner via mast cells [23,25,26]. That is, the production of the inhibitory mediator is activated and the self-inhibitory effect increases in a concentration-dependent manner when the histamine concentration is less than a threshold, but is suppressed and the self-inhibitory effect decreases, once the amount of histamine becomes larger than the threshold.…”
Section: Development Of Mathematical Modelmentioning
confidence: 99%
“…where α 1 is the positive constant implying the histamine concentration where the inhibition effect is the highest, and α 2 is the positive constant determining the highest level of inhibition effect (Fig 2B Right). For the inhibitory regulation, we assume that there exists a self-inhibition mechanism which is directly regulated in a histamine concentration-dependent manner via mast cells [23,25,26]. That is, the production of the inhibitory mediator is activated and the self-inhibitory effect increases in a concentration-dependent manner when the histamine concentration is less than a threshold, but is suppressed and the self-inhibitory effect decreases, once the amount of histamine becomes larger than the threshold.…”
Section: Development Of Mathematical Modelmentioning
confidence: 99%
“…1,2 We previously reported that blood coagulation potential is elevated in CSU and that histamine and agonists for tolllike receptors (TLRs) may synergistically induce tissue factor (TF) expression on vascular endothelial cells. 3,4 Immunohistochemical staining revealed TF expression by eosinophils in the lesion of CSU. 5 However, monocytes are considered to be the main source of TF in the blood, causing clot formation.…”
Section: Increase Of Tissue Factor Expression On the Surface Of Peripmentioning
confidence: 99%
“…To evaluate the effect of TF of monocytes on vascular permeability, we performed impedance analysis, which reflects the area of cellular adhesion and morphology on the electrodes as Cell Index (CI). 4 In Figure 2, the black line shows the decrease in CI, which reflects inter-cellular gap formation of histamine-and LPS-treated human umbilical vein epithelial cells (HUVECs) cultured on the electrodes in the presence of factor VIII-deficient plasma (positive control). A decrease in CI was also observed in the presence of sufficient numbers of TF-expressing monocytes from normal donors (10 4 cells/ well).…”
Section: Increase Of Tissue Factor Expression On the Surface Of Peripmentioning
confidence: 99%
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“…Activated eosinophils, hyper-expressing tissue factor, seem the main initiators of these phenomena, 4 although endothelial cells may concur as well. 5 The potential relevance of thrombin as well as of other activated coagulation factors in amplifying the release of histamine from mast cells and basophils, thus worsening the disease status, is suggested by several studies reporting the efficacy of anticoagulants in patients with severe CSU not responding to antihistamines at any dosage. 3 The humanized anti-IgE mAb, omalizumab, has become a main- probably represent a subset characterized by an IgG-mediated autoimmune mechanism directed to the high-affinity IgE receptor of to IgE.…”
Section: Baseline D-dimer Plasma Levels Correlate With Disease Activimentioning
confidence: 99%