Lipoprotein differential inhibition of lymphoproliferative response

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

Florencia, ITALIA

Congreso; 17º International Congress of Clinical Chemestry and Laboratory Medicine; 1999

 We investigated the effects of human low-density lipoprotein, LDL and high-density lipoprotein, HDL on human peripheral blood mononu-clear cells proliferative response to T-cell mitogens such as phytohae-magglutinin (PHA), anti-CD3 plus phorbol myristate acetate or by mixed lymphocyte culture. Lipoproteins were assayed in its native state or after mild oxidation by ultra-violet irradiation. LDL, oxLDL and HDL inhib-ited lymphocyte proliferation induced by phytohaemagglutinin while oxHDL produced no effect. In cultures containing HDL there was a higher proportion of resting lymphocytes while in those containing LDL there was a higher proportion of apoptotic cells.The addition of cyclooxygenase inhibitor indomethacin to cells in-cubated with lipoproteins and PHA completely abrogate the HDL, but not LDL, suppressive effect. Uppon measurement of prostaglandin E2 (PGE2) levels from cells cultured with HDL, we found a decrease in PGE2 accumulation. The addition of indomethacin to culture cells caused a dramatic inhibition of PGE2 production irrespectively of the presence of HDL. These findings indicate that HDL does not cause its immunosuppre-sive effect by increasing PGE2 production and suggests that indometha-cin does not produce its effect by cyclooxygenase inhibition. We specu-late that HDL could prevent atherosclerosis by inhibiting the prolifera-tive response of cells forming the atheroma.