EXPRESSION AND SECRETION OF LIPOCORTIN-1 IN GUT INFLAMMATION ARE NOT REGULATED BY PITUITARY-ADRENAL AXIS

Lipocortin 1 is considered a mediator of the anti-inflammatory actions of glucocorticoids. We have shown that this protein is overexpressed and secreted during an experimental colitis induced by intraluminal in jection of trinitrobenzenesulfonic acid (TNBS) in rats. We studied her e the in vivo regulation of lipocortin 1 expression and secretion in t his model, either by glucocorticoids using adrenalectomized or dexamet hasone-treated (3 mg/24 h) animals or by pituitary factors using hypop hysectomized animals. Inflammation was evaluated by measuring myeloper oxidase activity and by histological scoring of the damage. Lipocortin 1 was detected by immunoblotting, and its secretion was studied by in cubating colonic specimens in culture medium. In the colon of TNBS-inj ected animals, cumulative histological damage scores were increased in adrenalectomized and decreased in dexamethasone-treated animals compa red with control and hypophysectomized animals. The colons of all TNBS -injected animals (controls, adrenalectomized, dexamethasone treated, hypophysectomized) overexpressed and secreted lipocortin 1. In conclus ion, the induction of lipocortin 1 overexpression and secretion during this colitis occurs independently of glucocorticoids or pituitary fac tors.