VLDL modulates the cytokine secretion profile to a proinflammatory pattern

SAMPEDRO, MARÍA CECILIA; MOTRÁN, CRISTINA; GRUPPI, ADRIANA; KIVATINITZ, SILVIA CLARA

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

Academic Press

Año: 2001 vol. 285 p. 393 - 399

0006-291X

Human very-low-density lipoprotein (VLDL) inhibits DNA synthesis in lymphocytes activated by the nonspecific mitogen concanavalin A (Con A). We studied the effects of VLDL on lymphocyte activation (IL-2 receptor expression), cell cycle progression, and production of IL-2 and of IL-4 (a proinflammatory and an anti-inflammatory interleukin, respectively) to understand why an atherogenic lipoprotein inhibits cell proliferation. After 48 h of stimulation with the mitogen, VLDL decreased the population of cells bearing IL-2 receptor and the population of T-cells that progress through the cell cycle, increasing the population of T-cells in G0/G1. Cells cultured in the presence of Con A and VLDL produced higher levels of IL-2 and lower levels of IL-4 than cells cultured without VLDL. These results suggest that VLDL inhibits lymphocyte proliferation by reducing IL-2 receptor and enhancing the levels of IL-2. Probably, one atherogenic effect of VLDL is to modulate the cytokine secretion profile of lymphocytes to a predominantly proinflammatory response. Key Words: lipoprotein; T-cell proliferation; atherosclerosis;VLDL; IL-2.Key Words: lipoprotein; T-cell proliferation; atherosclerosis;VLDL; IL-2.