Human Polymorphonuclear Leukocyte (PMN) Priming/Activation by Acute Ethanol Intoxication

Abstract

The effects of chronic alcoholism on susceptibility to infections are well documented. Less is known on the effect of sporadic acute ingestion of ethanol on the immune system. One should not assume that it induces neutrophil function deficiency in vivo. One example of upregulation caused by ethanol treatment was described by Dorio (1): in vitro ethanol treatment of rat macrophages causes an acute rise in intracellular calcium, stimulates a small amount of Superoxide production, but it also inhibits concanavalin A- and phorbol ester-induced Superoxide formation. Acute ingestion of ethanol has been shown to affect some, but not all PMN functions: decreased adherence to surfaces, decreased delivery to inflammation sites, but no abnormality of chemotaxis, Superoxide generation, bacterial killing, or intracellular cAMP and cGMP levels (2,3). In other experimental studies in mice, both low dose (1 mg/Kg) and high dose (4 mg/Kg of body weight) of ethanol increased the number of sticking or plugging PMNs in sinusoids of the liver (4). A small decrease in phagocytosis has been detected by some (3), but not by others (2).