LEVANTAMENTO DE FUNGOS ECTOMICORRÍZICOS EM FLORESTA DE PINUS TAEDA EM CAÇADOR – SC

Abstract

Objective: Tumor necrosis factor-(alpha) (TNF(alpha)) is a pleiotropic cytokine exerting both inflammatory and cell death modulatory activity, and is thought to play a role in the pathogenesis of atherosclerosis. Studies in mice indicated that TNF(alpha) affects atherosclerosis minimally or not under conditions that allow fatty streak formation. Here, we examined the possible role of TNF(alpha) in advanced and complex atherosclerotic lesions. Methods and results: To induce atherosclerosis, TNF(alpha)-deficient (Tnf-/-) APOE*3-Leiden and control APOE*3-Leiden only mice were fed a cholesterol-rich diet. Comparable levels of plasma cholesterol and triglycerides and the systemic inflammatory parameters, serum amyloid A and soluble intercellular adhesion molecule-1 were found in APOE*3-LeidenTnf-/- and control mice. Although absence of TNF(alpha) did not affect the quantitative area of atherosclerosis, APOE*3-LeidenTnf-/- mice had a higher relative number of early lesions (46.1% vs. 21.4%) and a lower relative number of advanced lesions (53.9% vs. 78.6%, P=0.04). In addition, the advanced lesions in APOE*3-LeidenTnf-/- mice showed less necrosis (9.9(plus or minus)12.1% vs. 23.4(plus or minus)19.3% of total lesion area, P=0.04) and an increase in apoptosis (1.5(plus or minus)1.5% vs. 0.4(plus or minus)0.6% of total nuclei, P=0.03). Conclusions: Our data indicate that TNF(alpha) stimulates the formation of lesions towards an advanced phenotype, with more lesion necrosis and a lower incidence of apoptosis. (copyright) 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.