Abstract
Summary
A non-lethal, haptenic polysaccharide from K. pneumoniae, given intravenously to guinea pigs, produces a marked, but transient, elevation in plasma 17-hydroxycorticosteroids. Incubation of the polysaccharide with normal guinea pig plasma partially inactivates this response. The polysaccharide remaining in the circulating plasma 6 and 12 hours after intravenous injection shows a greater loss of this ACTH releasing property. Electrophoretic studies indicate that the polysaccharide is bound to plasma proteins, but there are marked differences in in vitro and in vivo binding with albumin. The bound polysaccharide, however, retains its haptenic qualities. These findings suggest that the bacterial polysaccharide undergoes little, if any, degradation but loses its 17-OHCS evoking capacity by combining with plasma proteins.
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