Delayed-Type Hypersensitivity as Revealed on the Footpads of Mice to Azobenzenearsonate-Acetyl Bovine Serum Albumin

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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.

Section: Discussionmentioning

confidence: 99%

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

Yoshino

Ellis²

1987

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“…We recently reported the induction of a comparatively pure delayed-type hy persensitivity (DTH) reaction on the footpad of mice, using ABA-AcBSA as an immunizing and challeng ing antigen. The DTH reaction was accompanied with only a very weak immediate reaction [32]. The in tensity of the DTH reaction with ABA-AcBSA was much stronger than those with BSA and azobenzenearsonate-conjugated lysozyme [32].…”

Section: Effect O F Preformed Air Pouch On Allergic Inflammation Withmentioning

confidence: 93%

Induction of an Allergic Air-Pouch Inflammation in Rats

Tsurufuji¹,

Yoshino²,

Ohuchi³

1982

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An allergic air pouch inflammation was induced on the dorsum of rats using azobenzenearsonate-conjugated acetyl bovine serum albumin as an antigen. Rats were immunized by intradermal injection with 5 mg of the antigen in 0.5 ml Freund’s complete adjuvant saline (1:1) emulsion. 9 days after the immunization 8 ml of air was injected subcutaneously on the dorsum, and 24 h later 4 ml of 2% sodium carboxymethyl cellulose solution containing 2 mg of the antigen was injected into the preformed air pouch to provoke the allergic inflammation. In addition to the histological observations of the inflammatory tissues of the pouch wall, time course studies on the volume of the inflammatory pouch fluid, on the number and species of inflammatory cells in the pouch fluid and on the wet weight of granulation tissues were carried out to characterize the nature of the inflammatory reaction, which was shown to be suitable as a model to perform quantitative measurements and biochemical analyses of the allergic inflammation.

“…The difference between the net increase in right and left footpad was recorded. See [8] for details. The values are the mean ± SEM.…”

Section: Resultsmentioning

confidence: 99%

“…We had found that indomethacin, a potent inhibitor of cyclooxyge nase, when applied locally, suppressed the allergic footpad inflammation in mice in a dose-dependent manner [8], Consequently, participation of arachido nate metabolites through the cyclooxygenase path way in the mechanisms leading to allergic inflamma tion was suggested. However, since it is difficult to collect inflammatory exudate from the footpad for the assay of prostaglandin E2, no quantitative correla tion of this suppression of allergic inflammation and a decrease in the level of prostaglandin E2 in the in flammatory footpad was possible.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies in this laboratory on allergic foot pad inflammation in mice revealed possible partici pation of cyclooxygenase products [8]. The present in vestigation was initiated to clarify the role of cyclo oxygenase metabolism in the development of allergic air pouch inflammation by comparing the effects of two drugs, indomethacin and dexamethasone, which inhibit arachidonic acid metabolism at different steps in the arachidonic acid transformation pathway.…”

Section: Introductionmentioning

confidence: 99%

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A Possible Role of Arachidonate Metabolism in Allergic Air Pouch Inflammation in Rats

Ohuchi¹,

Yoshino²,

Kanaoka³

et al. 1982

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The effect of indomethacin and dexamethasone on an allergic inflammation in rats, a novel model of allergic inflammation of an air pouch type, was examined. Indomethacin and dexamethasone exerted a dose-dependent inhibition of both the accumulation of inflammatory exudate and the migration of leukocytes into the exudate. And although prostaglandin E₂ levels in the exudate were lowered to the same extent by treatment with indomethacin and dexamethasone, inhibition of both exudate accumulation and leukocyte migration was more pronounced after treatment with dexamethasone. The differences in the effectiveness of indomethacin and dexamethasone in terms of inhibition of arachidonate metabolism in the allergic air pouch inflammation are discussed.