THE TNF-a SECRETION BY MACROPHAGES INDUCED BY THE LECTIN MNCF IS MAINTAINED UNDER ANTI-INFLAMMATORY CONDITION.

CECILIO N. T.(1), TOLEDO K. A.(1), ROQUE-BARREIRA M. C.(1)

(1)Department of Cellular and Molecular Biology, FMRP, USP, Ribeirão Preto, SP, Brazil

Glucocorticoids are known by their anti-inflammatory actions that include inhibition of the neutrophil migration, through mechanism that are poorly understood. Activated macrophages secret several inflammatory mediators, such as cytokines and neutrophil attractants. Among the macrophage derived attractants, a galactose-binding lectin, known as MNCF, is distinguished by its well demonstrated property of inducing neutrophil migration even in dexamethasone-pretreated mice. Several macrophage-derived inflammatory mediators stimulate macrophages themselves to secret cytokines. This fact motivated us to investigate if MNCF could exert similar activities on murine peritoneal macrophages, as well if the secreted products vary according the cells are obtained from mice that were treated, or not, with dexamethasone. MNCF was able to induce the secretion of IL-1b, IL-12p70, TNF-a, and NO by macrophages obtained from non-treated mice. When macrophages from dexamethasone-treated mice were stimulated with MNCF they did not produce IL-1b, IL-12p70 or NO, while TNF-asecretion was completely preserved. So, under anti-inflammatory circumstances MNCF-stimulated macrophages remain able to secret the citokine TNF-asuggesting that MNCF and TNF-a inflammatory actions can overcome the anti-inflammatory effects of glucocorticoids.

KEY WORDS: inflammation, lectin, MNCF, TNF-a, neutrophil migration, glucocorticoids

FINANCIAL SUPPORT: FAPESP

CORRESPONDENCE TO:

Karina Alves de Toledo, Departamento de Biologia Celular e Molecular, FMRP, USP, CEP 14049-900, Ribeirão Preto, SP. Email: karina@rpm.fmrp.usp.br