Antigenic Determinant Involved in Hypersensitivity of Infected Mice to Lipopolysaccharide of Salmonella

Sensitivity of mice to cell-wall lipopolysaccharide (LPS) extracted from certain strains of Salmonella was increased by infection with various strains of Salmonella typhimurium, Salmonella minnesota, and Salmonella enteritidis. Smooth or rough strains possessing a polysaccharide chain longer than that of the glucoseless mutant were capable of inducing this hypersensitivity. Infection with one strain sensitized animals to LPS from other strains. However, strains of Escherichia coli that had no antigen in common with rough-core polysaccharide could not induce hypersensitivity. Fractions containing either O side chains or LPS of the heptoseless mutants of Salmonella were ineffective in provoking hypersensitivity. Sensitization to smooth LPS by bacterial infection was prevented by prior administration to mice of rough LPS and not of the O side chain. These results indicate that the major antigenic determinant participating in this hypersensitivity is in the rough-core polysaccharide, presumably in the polysaccharide sequence from glucose-1 to glucose-2 of the rough core, but not in the O side chain or lipid A of LPS.