
Lipopolysaccharide and mouse virulence of Salmonella : O antigen is important after intraperitoneal but not intravenous challenge
Author(s) -
Saxén H.,
Hovi M.,
Mäkelä P.H.
Publication year - 1984
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1984.tb01245.x
Subject(s) - virulence , microbiology and biotechnology , lipopolysaccharide , salmonella , bacteria , antigen , biology , spleen , peritoneal cavity , enterobacteriaceae , immunology , escherichia coli , biochemistry , gene , genetics , anatomy
The quality of the O‐antigenic polysaccharide part of the cell wall lipopolysaccharide (LPS) is a virulence determinant in Salmonella strains: isogenic derivatives with antigen O‐4,12 have been shown to be more virulent than those with O‐6,7 when given intraperitoneally (i.p.) to mice. The O‐6,7 LPS activates complement by the alternative pathway more efficiently than does O‐4,12. We show here that the O‐6,7 (but not O‐4,12) bacteria were rapidly killed in the peritoneal cavity of the mice, resulting in approx. 100‐fold reduced numbers of bacteria reaching the liver; the subsequent rate of growth of the bacteria was not affected. After intravenous challenge, both O‐6,7 and O‐4,12 sister strains survived equally well in the liver and spleen and were of approximately equal virulence. We suggest that the rapid activation of complement by the O‐6,7 LPS leads to the killing of these bacteria by the peritoneal cells and thereby to reduced virulence.