Antiendotoxin Antibody Production of Mononuclear Cells in Multiply Injured Patients

In 1990 the definition of ‘translocation’ was expanded to include the passage of both viable and nonviable microbes and microbial products across an intact intestinal barrier [1]. Damage to the intestinal barrier causes increased permeability, which is responsible for bacterial components (e.g., endotoxins) entering the circulation [2-4]. Endotoxin is accepted as a potent trigger of the mediator cascade which can cause systemic inflammatory response syndrome (SIRS) and multiple organ failure. Multiply injured patients suffer from temporary endotoxemia, which is most probably due to translocation of endotoxin through the intestinal barrier [5, 6]. Endotoxins are T cell-independent antigens and can stimulate B cells directly [7]. Although there is an acquired immunological deficit after trauma [8], endotoxins are capable of stimulating the synthesis of antiendotoxin antibodies, increasing the amount of the specific IgM antibodies against endotoxins in the serum [5, 6]. However, the concentration of any substance in the blood is a result of production (synthesis or delivery into the blood) and consumption (degradation or removal from the blood). Therefore, this study examined the effect of temporary endotoxemia on peripheral mononuclear cells cultured after blood collection.