Abstract

Acute alcohol ingestion is commonly associated with burn injury. Both alcohol ingestion and burn injury produce immune suppression, but the combination of these factors on immune function has not been investigated. To study this combined effect, immune function was measured in rats with a 30% burn injury following a single ingestion of 2.4 g/kg of ethanol (EtOH) and compared to that of animals with burn injury only, animals with EtOH only, and animals with neither alcohol nor burn injury. Four days after ethanol and/or burn, animals receiving both ethanol and burn injury had significant suppression of in vivo chemotaxis and lymphocyte responsiveness to lipopolysaccharide (LPS) compared to animals receiving either burn injury alone or EtOH alone ( P < 0.05). There was no difference in responsiveness to concanavalin A (Con A). Serum corticosterone was significantly elevated by burn injury but not EtOH ingestion. EtOH treatment prior to injury caused a further increase in corticosterone level that was significantly associated with a decrease in immune function. These results indicate that a single EtOH exposure prior to burn injury produces greater immune suppression than does burn injury alone. This further decrease in immune function may contribute to increased susceptibility to infection and increased mortality in burn patients with acute EtOH ingestion.

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