Comparative actions of immunosuppressants, glucocorticoids and non-steroidal anti-inflammatory drugs on various models of delayed hypersensitivity and on a non-immune inflammation in mice.

Various models of delayed hypersensitivity (DH) were used in mice: contact hypersensitivity reactions to picryl chloride and oxazolone and reactions to methylated bovine serum albumin (MBSA) and sheep red blood cells (SRBC). Drugs of different classes were tested in these models by systemic treatment around the challenge period: non-steroidal anti-inflammatory drugs (cyclooxygenase inhibitors, and inhibitors of both cyclooxygenase and lipoxygenase); glucocorticoids and immunosuppressants (cyclosporin A. CsA; cyclophosphamide, Cy; methotrexate, Mtx; azathioprine, Aza).

Model of bronchial hyperreactivity after active anaphylactic shock in conscious guinea pigs.

A model of bronchial hyperreactivity at various times after an active anaphylactic shock in conscious guinea pigs is described. The bronchial inflammation was quantified in parallel by determination of the number of mononuclear cells, neutrophils, and eosinophils in bronchoalveolar lavage (BAL) fluids. The guinea pigs were sensitized by an intramuscular (i.

Antiallergic and anti-inflammatory action of tioxamast in rats. II. Anti-inflammatory action in vivo.

Tioxamast is an antiallergic drug that inhibits anaphylaxis in various models in rats, and it inhibits the release and synthesis of certain mediators of inflammation [see Tarayre et al., this issue]. Here we report that the drug also has an anti-inflammatory effect in vivo in various nonimmunological models in rats.

Antiallergic and anti-inflammatory action of tioxamast in rats. I. Antiallergic activity in vivo and in vitro.

Tioxamast (F 1865) is an antiallergic drug that, administered systemically, reduces anaphylaxis in various models in rats. This action is due mainly to the inhibition of the synthesis and release of certain mediators. Orally or intraduodenally administered tioxamast inhibits IgE-dependent passive cutaneous anaphylaxis (ED50 = 0.

Comparison of the cutaneous/systemic antiinflammatory activity ratios for desonide and hydrocortisone in various experimental models.

The ratios of antiinflammatory activity after oral administration (oral ED50/cutaneous ED50) for desonide (Locapred) and hydrocortisone (hydrocortisone acetate) were compared in various nonimmunological and immunological experimental models on mouse ears: edema induced by croton oil; primary irritation due to picryl chloride; the acute phase (6 h) and the beginning of the chronic phase (24 h) of inflammation due to cantharidin; delayed contact hypersensitivity to picryl chloride; and the semi-delayed (6 h) and delayed (24 h) phases of contact hypersensitivity to oxazolone. These investigations showed that, besides having a better antiinflammatory effect, desonide had a better ratio of local activity to systemic effect in all the models. In addition, by contrast with orally active doses, locally active doses did not induce any thymolytic effect.