Slow reacting substance in the exudate of allergic air pouch inflammation in rats

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Using an experimental model of allergic inflammation of air pouch type in rats, the mechanism of antiallergic action of β-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 β-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 β-antagonist, counteracted the effect of β-agonists. Serotonin-induced vascular permeability was also suppressed dose-dependently by treatment with β-agonists. Furthermore, vascular permeability in the postanaphylactic phase of the present experimental model was also suppressed by isoproterenol. These results indicate that β-agonists exert their antiallergic effect by inhibiting the reactivity of local vasculature to chemical mediators released from mast cells.

Section: Discussionmentioning

confidence: 99%

Mechanism of Antianaphylactic Action of β-Agonists in Allergic Inflammation of Air Pouch Type in Rats

Ohuchi¹,

Hirasawa²,

Takeda³

et al. 1987

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“…We have previously shown that humoral immunological responses including anaphylaxis and Arthus type hy persensitivity reactions may be involved in the early phase of this inflammation [40][41][42]. Therefore, dietary enrichment of (n-3)-fatty acids might influence the immunological responses before inflammatory re sponses occurred in the air pouch.…”

Section: Discussionmentioning

confidence: 99%

Effect of a Fish-Oil-Supplemented Diet on Inflammation and Immunological Processes in Rats

Yoshino

Ellis²

1987

The effect of a diet enriched in fish-oil-derived fatty acids including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DCHA) in inflammation and immunological processes in rats has been investigated. Rats on a normal chow diet were given 500 mg/kg/day EPA and 333 mg/kg/day DCHA by gavage over a period of 50 days. Control groups received water, oleic acid or safflower oil. Acute and chronic phases of inflammation induced by antigenic challenge with bovine serum albumin were examined in the rat air-pouch model. In rats receiving fish-oil-derived fatty acids, there was a reduced production of the arachidonic acid metabolites, prostaglandin E₂ and leukotriene B₄, in the exudate in the chronic phase of inflammation, but not in the acute phase. This was associated with an increased infiltration of leukocytes, especially monocytes and macrophages, in the chronic inflammatory phase. The fish-oil-supplemented diet showed no effect on the volume of inflammatory exudate, the amount of protein in the exudate and connective tissue proliferation. Carrageenin-induced paw edema in the animals was not influenced by the diet. There was no effect of the dietary fish oil on production of antibodies to bovine serum albumin in the rats. However, the diet appeared to suppress a delayed-type skin reaction in the animals. These studies suggest that fish-oil-derived fatty acids may modulate chronic inflammation and a cellular-mediated immunological reaction by reducing the synthesis of arachidonic acid metabolites.

“…In the anaphylactic phase of this model, we showed that the level of slow-reacting substance in the pouch fluid is high [48,49]. Such 5-lipoxygenase products might modulate the PAF formation by enhancing the expression of phospholipase A2 [50].…”

Section: Discussionmentioning

confidence: 99%

Platelet-Activating Factor in the Inflammatory Exudate in the Anaphylactic Phase of Allergic Inflammation in Rats

Watanabe¹,

Ohuchi²,

Sugidachi³

et al. 1987

Self Cite

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.