Contribution of various host factors to resistance to experimentally induced bacterial endotoxemia in calves.

The reactions of 15 calves to IV administered bacterial lipopolysaccharide was investigated and was correlated with the capacity of 2 host defense mechanisms. The calves had a wide range of changes in clinical response, total WBC count, plasma lactate dehydrogenase (LD) activity, reaction to intradermally inoculated lipid A, and rectal temperature response. The early rectal temperature response of an individual calf was correlated with plasma LD activity, indicating a relationship between cell damage and fever. The concentration of antibody against lipid A at the time of lipopolysaccharide inoculation was negatively correlated with the rectal temperature changes recorded during endotoxemia, suggesting a protective ability of antibody. The capacity of a plasma inhibitor of lipopolysaccharide-mediated clotting of limulus amebocyte lysate was correlated with increases in plasma LD activity. Therefore, antibody to lipid A probably is involved in protection of cattle during endotoxemia, but the plasma lipopolysaccharide inhibitor actually may potentiate lipopolysaccharide toxicity.