Fatty Acids, Platelets and Monocytes. Something to do with Atherogenesis

Abstract

A remarkable variation in monocyte activation among individuals was observed when blood from different people was incubated with lipopolysacchandes. To elucidate this phenomenon, we studied intracellular signals associated with monocyte activation. This was done by measuring induced thromboplastin synthesis.

An inhibitor of phospholipase A2 blocked the lipopolysaccharide induced synthesis of thromboplastin. Thus, release of arachidonic acid (20:4) seemed to be necessary to activate the monocytes. Nordihydroguaiaretic acid, a lipoxygenase inhibitor, had no effect on the monocyte activation in subjects with a low response to lipopolysacchar-ides (low responders); this contrasted with nearly 80 % inhibition in individuals with very sensitive cells (high responders).

Taking aspirin raised monocyte activation by an average of 50 %, this was caused by the effect of aspirin on the platelets.

Platelets enhanced the lipopolysaccharide activation of monocytes 2–3 fold. The high response phenomenon was partially due to platelets. When platelets in the blood of high responders were substituted with platelets from low responders, the monocyte activation fell by up to 70 %.

Fatty acids seemed to play a central role in the activation of monocytes. Intake of cod liver resulted in significant reduction of induced thromboplastin synthesis.

It is suggested that those who are high responders may be more susceptible to developing atherosclerosis.

Key Words:

• atherosclerosis
• fatty acids
• monocytes
• platelets
• thromboplastin