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Results for “Allergic inflammation”

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At least 19 recordsLinked to original sources

PubMed1990

Possible role for platelet-activating factor in neutrophil infiltration in allergic inflammation in rats.

Allergic inflammation was induced by injecting an antigen solution into an air pouch made on the dorsum of immunized rats with the antigen azobenzene-arsonate-conjugated acetyl bovine serum albumin. In this model, leukocyte infiltration into the pouch fluid was prominent 4-8 h after the antigen challenge. Most of the infiltrated leukocytes were neutrophils. Administration of the platelet-activating factor (PAF) antagonists such as CV-3988 and L-652,731 into the air pouch 15 min before and at the time of the antigen challenge failed to suppress leukocyte infiltration at 8 h. However, when the PAF antagonist was injected into an air pouch 4 h after the antigen challenge, neutrophil infiltration at 8 h was suppressed in a dose-dependent manner. Combined treatment with the 5-lipoxygenase inhibitor AA861 and the PAF antagonist did not potentiate the effect of the PAF antagonist, suggesting that participation of leukotriene B4 in neutrophil infiltration in this model is negligible. Eosinophil infiltration was very weak at 8 h, and the PAF antagonist showed no significant effect. At 8 h, the PAF level in the serum of the immunized rats was significantly higher than that of the nonimmunized rats. Intravenous administration of the PAF antagonist 15 min before the antigen challenge suppressed leukocyte infiltration more effectively than local administration into the pouch. These results indicate that PAF plays a significant role in neutrophil infiltration in allergic inflammation.

Animals↗

PubMed1991

Characterization of methylated bovine serum albumin-induced allergic inflammation in rats.

An air pouch type allergic inflammation in rats was induced using an insoluble cationic protein, methylated bovine serum albumin (MeBSA), as an antigen. Changes in vascular permeability, local tissue edema, histamine contents in the pouch fluid, and number of infiltrated leukocytes and chemotactic activity in the pouch fluid were analyzed during an 8-hour period after injecting the antigen solution into the air pouch of the immunized and nonimmunized rats. Vascular permeability during the first 30-min interval in the immunized rats was higher than that in the nonimmunized rats, reflecting a higher histamine level in the pouch fluid. However, both the increase in vascular permeability and histamine level in the immunized rats in this period were much lower than those induced by a soluble, noncationic antigen, azobenzenearsonate-conjugated acetyl bovine serum albumin. In the MeBSA-induced allergic inflammation model, a second peak of vascular permeability was induced at 2 h, and local tissue edema formation became apparent at 2 h, reaching a plateau at 4 h. A prominent increase in leukocyte infiltration, especially neutrophils, into the pouch fluid was induced at 4 h in accordance with an increase in chemotactic activity in the pouch fluid. These observations indicate that the acute phase of MeBSA-induced allergic inflammation is characterized by a weak anaphylactic response and a prominent neutrophil infiltration.

Animals↗

PubMed1991

A role of peripheral leukocytes in vascular permeability and edema formation in air pouch type allergic inflammation in rats.

Using an air pouch type allergic inflammation model in rats, a role of circulating leukocytes in allergic inflammation responses was investigated by comparing normal rats with peripheral leukocytopenia rats induced by cyclophosphamide treatment. In the leukocytopenia rats, vascular permeability, edema formation, leukocyte infiltration into the pouch fluid, neutrophil chemotactic activity in the pouch fluid occurred both at the early phase (4 h) and the late phase (8 h) after the antigen challenge were decreased. However, edema formation induced by intradermal injection of arachidonate metabolites, serotonin, or platelet activating factor was not suppressed at all in the leukocytopenia rats. A possible role of peripheral leukocytes in allergic and non-allergic inflammation is discussed.

Animals↗

PubMed1987

Platelet-activating factor in the inflammatory exudate in the anaphylactic phase of allergic inflammation in rats.

Using a model of allergic inflammation of air pouch type in rats, the platelet-activating factor (PAF) in the pouch fluid in the anaphylactic phase was analyzed. Anaphylactic reaction was induced by injecting an antigen (azobenzene-arsonate-conjugated acetyl bovine serum albumin) solution into a subcutaneous air pouch preformed on the dorsum of immunized rats. The pouch fluid was collected 30 min after the antigenic challenge, and chloroform extract was subjected to normal phase high-performance liquid chromatography to isolate two fractions, PAF and lyso-PAF. In the pouch fluid, however, there was little activity of PAF as examined by the aggregation of guinea pig platelets. The lyso-PAF fraction obtained was acetylated to PAF chemically with pyridine and acetic anhydride. This acetylated lyso-PAF fraction induced the aggregation of guinea pig platelets, which was inhibited dose-dependently by a PAF antagonist, CV-3988. The amount of lyso-PAF in the pouch fluid of the immunized group in the anaphylactic phase was significantly higher than that of the nonimmunized group. When (3H-)PAF was incubated with the supernatant fraction of the pouch fluid it was metabolized into lyso-PAF time-dependently. The significance of the higher level of lyso-PAF in the pouch fluid in the anaphylactic phase of allergic inflammation is discussed.

Adenosine Diphosphate↗

PubMed1989

The role of platelet activating factor in allergic inflammation.

It is becoming increasingly apparent that platelet activating factor (PAF) is an important mediator in allergic disease. It is synthesized by a variety of cells including those which are thought to participate in the inflammatory process. In turn, PAF may stimulate these cells which further propagates the inflammatory process. Furthermore, PAF can mimic most of the characteristics which are relevant in allergic inflammation and PAF can produce effects comparable to that produced by antigen in animal models of allergic inflammation and in man. Other evidence to support the involvement of PAF in allergic disease has also arisen with the advent of PAF antagonists. Many PAF-induced responses can be attenuated by these agents and many antigen-induced responses in both animal models and in man can also be attenuated by PAF antagonists. This review attempts to summarize the results from studies which have investigated the role of PAF in allergic inflammation and the effects of PAF antagonists against both PAF and allergic-induced responses.

Animals↗

PubMed1990

Inhibition by dexamethasone of histamine production in allergic inflammation in rats.

In an allergic inflammation model of air pouch type in rats, histamine level in the pouch fluid and histidine decarboxylase activity of pouch wall tissues in the postanaphylaxis phase were increased. Although treatment with dexamethasone failed to inhibit histamine release from mast cells in the anaphylaxis phase, histamine production in the postanaphylaxis phase was inhibited dose dependently. Histamine production-increasing activity in the pouch fluid collected 8 h after the Ag challenge, which was estimated by an activity to stimulate histamine production by bone marrow cells, was decreased by the administration of dexamethasone at the time of the Ag challenge. The addition of steroidal antiinflammatory drugs, dexamethasone, prednisolone, or hydrocortisone, into the incubation medium inhibited the pouch fluid-induced histamine production by bone marrow cells. Hydrocortisone mesylate antagonized the inhibitory effect of dexamethasone on histamine production by bone marrow cells. However, hydrocortisone mesylate failed to recover the decrease in histamine production-increasing activity of the pouch fluid collected from dexamethasone-treated rats. In addition, the dialyzed sample of pouch fluid obtained from dexamethasone-treated nonsensitized rats did not reduce the stimulated histamine production by the pouch fluid sample obtained from the sensitized rats. However, increase in histamine production of bone marrow cells stimulated by the pouch fluid was not inhibited by cyclosporin A that inhibited histamine production induced by Con A. This observation indicates that the pouch fluid has no effect to induce production of the histamine production-increasing factor by bone marrow cells. Consequently, it is suggested that dexamethasone inhibits not only the production of histamine production-increasing factor but also the response of histamine-producing cells to this factor.

Animals↗

PubMed1988

Metabolism of leukotriene C4, D4 and E4 in allergic inflammation in rats.

Using an allergic inflammation model of air pouch type in rats, levels of peptide-leukotriene (LT) C4, D4 and E4 in the pouch fluid were measured chromatographically, and peptide-LT metabolizing activities in the pouch fluid in the anaphylactic phase were examined. 10 min after injection of an antigen (azobenzene arsonate-conjugated acetyl bovine serum albumin) solution into a preformed air pouch on the back of the immunized rats, LTC4 level in the pouch fluid was the highest, followed by LTD4 and LTE4. At 30 min, the order of the level was reversed to LTE4 greater than LTD4 greater than LTC4, and total amount of peptide-LTs (LTC4 + LTD4 + LTE4) was the highest. Supernatant fraction of the pouch fluid collected 30 min after the antigenic challenge, converted [3H]LTC4 into [3H]LTD4, and [3H]LTD4 into [3H]LTE4 in time- and concentration-dependent manner. [3H]LTE4 was not metabolized under these conditions. Heat denaturation of the pouch fluid diminished the conversion of [3H]LTC4 into [3H]LTD4, and [3H]LTD4 into [3H]LTE4. In the granule fraction of purified mast cells, no metabolic activity of [3H]LTs was found. In intact mast cells as well as degranulating mast cells, a small but significant amount of [3H]LTC4 was metabolized into [3H]LTD4 and [3H]LTE4. In contrast, rat serum showed potent metabolizing activities of peptide-LTs. Since plasma exudation into the pouch is very prominent in the anaphylactic phase in this model, peptide-LT metabolizing activities in the pouch fluid are suggested to be attributable to plasma leaked into the pouch during the anaphylactic phase.

Anaphylaxis↗

PubMed1987

Role of endogenous histamine in postanaphylactic phase of allergic inflammation in rats.

Role of endogenous histamine in postanaphylactic phase of allergic inflammation was examined by using a rat model of allergic inflammation of air pouch type. Histamine in the exudate revealed a biphasic increase. The anaphylactic increase was followed by rapid decrease and then by a gradual rising in postanaphylactic phase with the maximum attained around 24 hr after the antigenic challenge. It again decreased gradually. The histamine increase in the postanaphylactic phase was accompanied by the increase of histidine decarboxylase activity in inflammatory tissues. Local administration of pyrilamine, an H1 antagonist, together with either methysergide, a serotonin antagonist, or cimetidine, an H2 antagonist, was unable to inhibit vascular permeability response in the postanaphylactic phase. When histaminase was administered locally in the postanaphylactic phase to reduce histamine in the exudate, neutrophil accumulation in the exudate was enhanced without any change in exudate accumulation. Enhancement of the neutrophil accumulation was also inducible with local administration of cimetidine but not with pyrilamine. Local administration of histamine inhibited the neutrophil accumulation dose-dependently. These results suggest that endogenous histamine released in the postanaphylactic phase contributes to downward regulation of neutrophil accumulation in the inflammatory site without affecting the vascular permeability.

Amine Oxidase (Copper-Containing)↗

PubMed1988

[Inhibitory effect of AD-1590, a non-steroidal anti-inflammatory drug, on allergic inflammation in mice and rats].

Effect of AD-1590 on allergic inflammations was investigated. AD-1590 and indomethacin at an oral dosage as high as 32 mg/kg did not show any significant inhibitory activity on rat passive cutaneous anaphylaxis, a type-I allergy, although prednisolone and cyproheptadine produced strong inhibition. Against rat adjuvant arthritis, type-III and -IV allergies, AD-1590 showed potent prophylactic (2 and 4 mg/kg/day) and therapeutic (0.4-1 mg/kg/day) effects when given orally once a day for 3 weeks beginning from just before and for 1 week starting from 14 to 18 days after adjuvant inoculation, respectively; however, its prophylactic and therapeutic potencies were about one-fourth and one-fifth, respectively, that of indomethacin. The arthritis was strongly inhibited with prophylactic treatment of prednisolone (1 mg/kg/day) or cyproheptadine (40 mg/kg/day). On the other hand, prednisolone (ED50 = 0.0119 mg/ear, topical) showed strong activity in inhibiting mouse contact hypersensitivity to oxazolone (ear edema), a type-IV allergy, but cyproheptadine only had weak activity. AD-1590 (0.318 mg/ear) and indomethacin (0.699 mg/ear) produced rather strong inhibition; in particular, AD-1590 produced almost complete inhibition at high dosages, whereas most of the non-steroidal anti-inflammatory drugs (NSAID) tested showed weak inhibition or a partial inhibition of about 50% even at the highest dosage. The oral potency of AD-1590 was about 2 and 100 times those of indomethacin and ibuprofen, respectively. These results demonstrate that in allergic inflammation, the pharmacological properties of AD-1590 are somewhat different from those of other NSAID and different from those of prednisolone and cyproheptadine.

Animals↗

PubMed1987

Recurrence of an allergic inflammation of air-pouch type in rats and possible participation of prostaglandin E2.

The recurrence of allergic inflammation, as examined by exudate accumulation, infiltration of polymorphonuclear leukocytes into the exudate, edema formation, vascular permeability and prostaglandin E2 levels in the exudate, was induced by injecting the antigen, azobenzene arsonate-conjugated acetyl bovine serum albumin, into the capsule of the proliferative granulation tissue which had been formed by the first-time antigenic challenge injection into an air pouch in the dorsum of the sensitized rat. The recurrence of the allergic inflammation 4 and 24 h after the antigenic challenge was inhibited dose-dependently by treatment with cyclooxygenase inhibitors, suggesting the possible participation of cyclooxygenase products, especially prostaglandin E2. The difference in the allergic inflammatory responses induced by the first-time antigenic challenge and the second-time antigenic challenge was discussed from the viewpoint of chemical mediators.

Animals↗

PubMed1990

The neutrophil and chronic allergic inflammation. Immunochemical localization of neutrophil elastase.

To test whether neutrophils infiltrate and degranulate in areas of chronic respiratory allergic inflammation, we developed an indirect immunofluorescence technique to localize neutrophil elastase in formalin-fixed, paraffin-embedded tissues. The affinity-purified antielastase stained only neutrophils on peripheral blood buffy coat smears, and in lung tissue from patients with pneumonia. We examined tissue specimens from four patients with fatal asthma, 10 patients with chronic sinusitis, and 10 patients with nasal polyposis for the presence of elastase, as well as eosinophil granule major basic protein (MBP). Neutrophil infiltration and extracellular elastase deposition in association with damage to respiratory epithelium were generally sparse in most specimens; the exceptions were one patient with asthma, one patient with chronic sinusitis, and two patients with nasal polyposis. In contrast, eosinophil infiltration and extracellular MBP deposition were generally marked in most specimens; the exceptions were one patient with asthma and one patient with nasal polyps where extracellular MBP deposition did not coincide with damage to respiratory epithelium. The results suggest that the neutrophil does not usually infiltrate tissues showing allergic inflammation; however, on occasion, it may participate in these inflammatory reactions.

Adult↗

PubMed1992

Analysis of the leukotriene D4 receptor in the granulation tissue of allergic inflammation in rats.

Leukotriene (LT) D4 receptor in the granulation tissue formed in the air pouch-type allergic inflammation model in rats was analyzed. Membrane preparation of the granulation tissue obtained 3-9 days after the antigen challenge has specific binding sites of [3H]LTD4. Scatchard analysis showed that the affinity (Kd) and the density (Bmax) were not changed among the granulation tissue obtained 3-9 days after the antigen challenge. The Kd value in the granulation tissue (0.90 +/- 0.12 nM) was close to that in the rat lung (1.00 +/- 0.24 nM) and the guinea pig lung (0.86 nM). On the other hand, Bmax (62 +/- 8 fmol/mg protein) in the granulation tissue was higher than that in the rat lung (21 +/- 4 fmol/mg protein) but was far less than that in the guinea pig lung (405 fmol/mg protein). LTC4 and LTE4 inhibited the binding of [3H]LTD4 to the membrane preparation of the granulation tissue in a concentration-dependent manner. IC50 of LTC4 and LTE4 were 1 x 10(-7) and 2 x 10(-7) M, respectively. A guanine nucleotide, guanyl-5'-yl-imido-diphosphate (GppNHp), reduced [3H]LTD4 binding to the membrane preparation of the granulation tissue suggesting that LTD4 receptors in the granulation tissue are associated with G proteins. These results indicate that LTD4 binding sites in the granulation tissue are high affinity receptors for LTD4. A possible role of LTD4 in the recurrence of allergic inflammation in the chronic phase is discussed.

Animals↗

PubMed1992

Eosinophils express interleukin 5 and granulocyte macrophage-colony-stimulating factor mRNA at sites of allergic inflammation in asthmatics.

IL-5 and granulocyte macrophage-colony-stimulating factor (GM-CSF) are important regulators of eosinophil survival, proliferation, and effector function. To determine whether IL-5 and/or GM-CSF are generated by eosinophils at sites of allergic inflammation, we have used in situ hybridization with 35S-labeled RNA probes to study the expression of IL-5 and GM-CSF mRNA in bronchoalveolar lavage (BAL) eosinophils derived from asthmatics (n = 5) before and after endobronchial allergen challenge. Endobronchial allergen challenge induced a significant airway eosinophilia (pre-allergen challenge 0.6 +/- 0.5% eosinophilia vs post-allergen challenge 48.2 +/- 25.6% eosinophilia). Post-allergen challenge eosinophils expressed IL-5 and GM-CSF mRNA, but did not express IL-1 beta or IL-2 mRNA. To determine whether the IL-5 mRNA-positive cells coexpressed GM-CSF mRNA, double mRNA labeling experiments with a digoxigenin-11-UTP nonradioactive labeled IL-5 RNA probe and a GM-CSF 35S-labeled RNA probe were performed. These studies demonstrated that individual eosinophils expressed one of four cytokine mRNA profiles (IL-5+, GM-CSF+, 34 +/- 13%; IL-5+, GM-CSF-, 34 +/- 5%; IL-5-, GM-CSF+, 11 +/- 9%; IL-5-, GM-CSF-, 21 +/- 25%). The expression of IL-5 and GM-CSF by eosinophils at sites of allergic inflammation in asthmatics may provide an important autocrine pathway, maintaining the viability and effector function of the recruited eosinophils.

Adolescent↗

PubMed1991

Structural cell-derived cytokines in allergic inflammation.

Based on observations of fluctuations in progenitors for inflammatory cells during allergic responses, we have proposed that a primary determinant of allergic inflammation involves microenvironmental influences on hemopoietic cell differentiation and phenotype; in addition, as a corollary of this, inflammatory cell burden is proposed as an important indicator of the severity and pattern of the inflammatory process in allergy. The studies outlined here focus on the effects of epithelial-cell- and fibroblast-derived cytokines on granulocytic and monocytic cell differentiation and activation in models involving allergic reactions in the upper and lower airways. Pure cultures of nasal or bronchial epithelial cells or fibroblasts are observed to give rise to cytokines important in inducing the differentiation of basophils, eosinophils, neutrophils and monocyte/macrophages. Gene expression, production and secretion of granulocyte/macrophage-colony-stimulating factor, interleukin-6 (IL-6) and IL-8 can be demonstrated in vitro and in vivo. Up-regulation of gene expression and production of these cytokines, which are important in inducing basophil, eosinophil and neutrophil/macrophage differentiation in several assays, is seen with IL-1 and the neuropeptide substance P; conversely, inhibition of cytokine production by structural cells is observed after pretreatment with corticosteroids in vitro, paralleling in vivo effects. Other modulatory effects also examined include: antiallergic compounds, which may affect posttranscriptional events in cytokine production, and heavy metal ions, which can also induce changes in gene expression. Structural-cell-derived extracellular matrices appear also to be important both in mast cell differentiation and in macrophage cytokine gene expression, both of which potentially feedback upon chronic allergic inflammatory processes, leading to their perpetuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Bronchi↗

PubMed1987

Mechanism of antianaphylactic action of beta-agonists in allergic inflammation of air pouch type in rats.

Using an experimental model of allergic inflammation of air pouch type in rats, the mechanism of antiallergic action of beta-agonists was examined. In this model an immediate increase in vascular permeability and histamine level in the pouch fluid was observed after injecting the antigen (azobenzene arsonate-conjugated acetyl bovine serum albumin) solution into the preformed air pouch on the back of the sensitized rats. The same type of reaction was inducible by injecting anti-rat IgE into the preformed air pouch, but not IgG2a. This fact indicates that the immediate increase in vascular permeability and histamine level is an IgE-mediated anaphylactic reaction. When beta-agonists such as isoproterenol, procaterol and salbutamol were injected into the air pouch together with the antigen, the anaphylactic increase in vascular permeability was suppressed dose-dependently without concomitant decrease in histamine level in the pouch fluid. In contrast, disodium cromoglycate, an inhibitor of degranulation of mast cells, the anaphylactic vascular permeability increase was suppressed in parallel with a decrease of the histamine level. Propranolol, a beta-antagonist, counteracted the effect of beta-agonists. Serotonin-induced vascular permeability was also suppressed dose-dependently by treatment with beta-agonists. Furthermore, vascular permeability in the postanaphylactic phase of the present experimental model was also suppressed by isoproterenol. These results indicate that beta-agonists exert their antiallergic effect by inhibiting the reactivity of local vasculature to chemical mediators released from mast cells.

Adrenergic beta-Antagonists↗

PubMed2026

Prophylactic Inhaled Pattern Recognition Receptor Agonists Reprogram Lung Epithelial Response and Prevent Type 2 Allergic Inflammation.

Prophylactic inhalation of the synergistic agents ODN M362 and Pam2CSK4 ("Pam2ODN") protects mice against allergic lung disease, including allergic inflammation caused by house dust mite (HDM). By preventing sensitization, Pam2ODN reduces HDM-induced eosinophilic and lymphocytic inflammation. How Pam2ODN affects interactions among lung epithelial cells, dendritic cells, and T cells to prevent eosinophilic lung inflammation remains unclear. In the present study, we show that a single inhaled dose of Pam2ODN before HDM sensitization reduces airway Th2 polarization without affecting Th1 or Treg responses. Furthermore, Pam2ODN pretreatment inhibits the recruitment of lung monocyte-derived dendritic cells (moDCs) and conventional Type 2 dendritic cells (DC2s), while preventing the HDM-induced decrease in conventional Type 1 dendritic cells (DC1s). Bulk RNA-seq of the whole lung reveals that Pam2ODN pretreatment restricts the expression of proinflammatory transcripts induced by HDM sensitization. This tolerogenic effect is also reflected at the single-cell level in lung epithelial cells, where proinflammatory transcripts, pathways, and chromatin accessibility are inhibited. These results indicate that Pam2ODN reprograms lung epithelial cells to attenuate allergen-induced Th2-promoting cytokines and DCs while maintaining the population of protective DC1s. These findings suggest a strategy to mitigate chronic allergic lung diseases.

Animals↗

PubMed1989

Occurrence of histamine-production-increasing factor in the postanaphylactic phase of allergic inflammation.

Experimental study on histamine liberation in a postanaphylactic phase of allergy was carried out employing an air pouch model of allergic inflammation in rats. The antigen used was azobenzenearsonate-conjugated acetyl bovine serum albumin. Synthesis and liberation of histamine took place in the inflammatory pouch in the dorsum of the allergic rats, and brought about a gradual rise in the histamine level in the pouch fluid with a peak at 24 h after the antigen challenge. The time course of the histamine level in the pouch fluid was quite similar to that of histidine decarboxylase activities in the inflammatory tissues. alpha-Fluoromethylhistidine reduced the histamine level in the postanaphylactic phase, although it had been ineffective in the anaphylactic phase. A substance capable of increasing histamine production by bone marrow cells was found in the pouch fluid of allergic rats, while it was absent in the normal rat serum and pouch fluid of nonsensitized rats. The histamine-production-increasing activity rose until 24 h after the antigen challenge, but fell at 48 h in parallel with changes both of histamine levels in the pouch fluid and histidine decarboxylase activity in inflammatory tissues. The histamine-production-increasing factor is thought to be a protein, since it was inactivated by treatment with heat (70 degrees C for 30 min) or trypsin. Its molecular weight was estimated to be between 25,000 and 40,000.

Anaphylaxis↗

PubMed1986

Vascular permeability responses and the role of prostaglandin E2 in an experimental allergic inflammation of air pouch type in rats.

Rats were sensitized with azobenzene arsonate-conjugated acetyl bovine serum albumin. An allergic inflammation was induced in the preformed air pouch in the dorsum of the sensitized rats by injecting the antigen dissolved in a 2% sodium carboxymethyl cellulose solution into the air pouch. Time course changes of vascular permeability, accumulated pouch fluid volume and prostaglandin E2 (PGE2) levels in the pouch fluid were compared in sensitized and non-sensitized rats to characterize the allergic inflammatory reaction. Effects of three cyclo-oxygenase inhibitors (indomethacin, diclofenac sodium and tiaprofenic acid) on vascular permeability and accumulated pouch fluid volume 4 and 24 h after the immunological challenge injection were examined to elucidate a possible role of PGE2 in the inflammatory response. Four h after initiating the allergic reaction, although the level of PGE2 in the pouch fluid reached a high level, the vascular permeability response, measured over the period 3.5-4 h, was not suppressed by treatment with the three cyclo-oxygenase inhibitors and neither was the pouch fluid volume measured over the period 0-4 h. However, vascular permeability and accumulated pouch fluid volume at 24 h were suppressed by the cyclo-oxygenase inhibitors in a dose-dependent manner. These observations suggest that in this model, endogenous PGE2 does not affect oedema formation measured at 4 h. However, oedema formation measured at 24 h may be dependent on PGE2 generation.

Animals↗