Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Qu, Xiao Fei; Hayashi, Masahiko; Yamaki, Kohji; Oh‐ishi, Sachiko

doi:10.1254/jjp.52.500

Cited by 7 publications

(4 citation statements)

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“…It has also been reported to enhance the adhesion of eosinophils to endothelial cells through the upregulation of cell adhesion molecules [22], degranulation of eosinophils [23], and vascular permeability [24,25]. Y-24180, a PAF receptor antagonist, inhibited ear swelling in both IPR and LPR in a dose-dependent manner ( fig.…”

Section: Discussionmentioning

confidence: 99%

Differential Effect of Antiallergic Drugs on IgE-Mediated Cutaneous Reaction in Passively Sensitized Mice

et al. 2000

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We investigated the effect of several antiallergic agents on murine IgE-mediated biphasic cutaneous reaction. Mice were passively sensitized by an intravenous injection of monoclonal anti-dinitrophenol (anti-DNP) IgE antibody. Skin reaction was elicited by an epicutaneous challenge of dinitrofluorobenzene (DNFB) and occurred biphasically with immediate-phase response (IPR) and late-phase response (LPR) at 1 and 24 h, respectively. Classical histamine H1 receptor antagonists and some chemical mediator-release inhibitors, such as diphenhydramine and terfenadine, inhibited IPR, but not LPR. In contrast, leukotriene B₄ (LTB₄) receptor antagonist (ONO-4057) inhibited LPR only. Antagonists for LTC₄, D₄, E₄ receptor (ONO-1078) and platelet-activating factor (PAF) receptor (Y-24180) significantly inhibited both IPR and LPR, similarly to prednisolone. We recently found that a third-phase inflammatory reaction with marked infiltration of eosinophils (named very-late-phase response; vLPR), which is supposed to be a more important reaction in allergic diseases, was induced, peaking at day 8 following IPR and LPR in this model. The effect of these drugs on the triphasic skin reaction can be scored based on efficacy against IPR / LPR / vLPR; +/+/+ (prednisolone, a PAF receptor antagonist Y-24180, cyclosporin A and FK-506), +/–/– (diphenhydramine), +/+/– (azelastine and LT receptor antagonist ONO-1078), and –/+/+ (an LTB₄ receptor antagonist ONO-4057). Thus the inhibitory effect on vLPR as well as LPR may relate to the inhibition of eosinophil function mediated by LTB₄ and PAF and/or T cells. These findings may provide the basis for a treatment modality using various antiallergic agents in allergic disease.

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Section: Discussionmentioning

confidence: 99%

Differential Effect of Antiallergic Drugs on IgE-Mediated Cutaneous Reaction in Passively Sensitized Mice

et al. 2000

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“…As mouse dorsal skin is too thin for injection, we developed a paw edema model to assess the vascular permeability in crease in the mouse (4).…”

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confidence: 99%

“…Sixty minutes later, the mice were exsanguinated, and both feet were removed. Dye extraction was done as previously reported, and the amount of ex udated dye in the control foot which received vehicle solution was subtracted from that at the inflamed site, as previously described (4).…”

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confidence: 99%

“…Furthermore, 72-hr edema was also sig nificantly suppressed by AA-861 (2,3,5 trimethyl-6-(12-hydroxy-5,10-dodecadinyl)-1,4 benzoquinone, a gift from Takeda Co., a 5 lipoxygenase inhibitor). The doses of drugs used were estimated from the information re ported in previous papers (4,6,7). However, doses of 5 mg/kg of mepyramine or 80 mg/kg of AA861 might be too high to manifest speci fic inhibition, and these doses might express non-specific in vivo suppression in this mouse edema.…”

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Vascular Permeability Increase in the Mouse Paw during the Passive Anaphylaxis Reaction

Yamaki

Oh‐ishi

1991

Japanese Journal of Pharmacology

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ABSTRACT-Assessment of mouse paw edema induced by the passive allergic reac tion was made by the previously reported dye-leakage method. The edema was in duced by the injection of antiserum against ovalbumin into the paw, followed by the intravenous injection of ovalbumin 10 min before or 72 hr later. The latter reaction may be mainly mediated by heat-labile IgE. Both of the edemas were suppressed by pretreatment with mepyramine, methysergide, PAF-antagonists, or dexamethasone, and the latter suppressed by the lipoxygenase inhibitor AA-861, suggesting that hista mine, serotonin, PAF, and leukotrienes are involved in exudate formation in these edemas.Vascular permeability increase is a phe nomenon seen in the initial phase of acute in flammation and allergy; and assessment of the reaction was previously made in the skin, paws or pleural cavity of various experimental animals by the use of pontamine sky blue dye exudation (1-3). As mouse dorsal skin is too thin for injection, we developed a paw edema model to assess the vascular permeability in crease in the mouse (4).In the present work, we applied the method to study the allergic exudation in the mouse paw in which the passive subcutaneous anaphylactic reaction had been induced (5).Male 5-week-old ICR mice (Shizuoka Laboratory Animal Center, Hamamatsu) were used for the induction of inflammation.Female 5 8-week-old Balb/c mice were used for antiserum production; i.e., they were in traperitoneally injected with 50 pg of ovalbu min and 15 mg of alum and then boostered with 5,ug ovalbumin on the 10th day. Anti sera were obtained on the 17th day.Two models were devised for the passive anaphylaxis reaction in the mouse paw. [1] 10 min anaphylaxis: ICR mice were anesthetized with pentobarbital sodium (50 mg/kg), and ovalbumin (4 mg/kg) and pontamine sky blue (PSB, 60 mg/kg) were injected into a tail vein; and then 10 min later, antiserum to oval bumin was injected into the foot pad (50,ul vehicle was injected into the other foot). Sixty minutes later, the mice were exsanguinated, and both feet were removed.[2] 72-hr anaphyl axis: ICR mice were injected with 50,ul of va rious dilutions of antiserum into the paw under light ether anesthesia (50 ,ul of vehicle was injected into the other foot); and 72 hr later, the mice were anesthetized with pento barbital sodium (50 mg/kg), and then ovalbu min (4 mg/kg) and PSB (60 mg/kg) were in

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Pharmacology of ABT-491, a highly potent platelet-activating factor receptor antagonist

Albert

Magoc

Tapang

et al. 1997

European Journal of Pharmacology

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Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Abstract: Abstract-Vascular permeability increase induced by histamine, bradykinin, platelet activating factor (PAF), or phorbol myristate acetate (PMA) in the mouse paw was assessed by the dye leakage method.

Cited by 7 publications

References 6 publications

Differential Effect of Antiallergic Drugs on IgE-Mediated Cutaneous Reaction in Passively Sensitized Mice

Differential Effect of Antiallergic Drugs on IgE-Mediated Cutaneous Reaction in Passively Sensitized Mice

Vascular Permeability Increase in the Mouse Paw during the Passive Anaphylaxis Reaction

Pharmacology of ABT-491, a highly potent platelet-activating factor receptor antagonist

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