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INFLUENCE OF THE CELL SURFACE LIPOPOLYSACCHARIDE STRUCTURE OF SALMONELLA TYPHIMURIUM ON RESISTANCE TO INTRACELLULAR BACTERICIDAL SYSTEMS
Author(s) -
Tagesson Christer,
Stendahl Olle
Publication year - 1973
Publication title -
acta pathologica microbiologica scandinavica section b microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0365-5563
DOI - 10.1111/j.1699-0463.1973.tb02232.x
Subject(s) - biochemistry , myeloperoxidase , chemistry , bacterial cell structure , intracellular , mutant , lipopolysaccharide , bacteria , microbiology and biotechnology , biology , gene , genetics , immunology , inflammation , endocrinology
The virulent Salmonella typhimurium 395 MS and R mutants derived from it that have deficiencies in their cell wall lipopolysaccharide (LPS) were examined for sensitivity to different bactericidal systems operating within the polymorphonuclear leucocyte: (1) the lysosomal granule fraction (8200 × g), (2) the myeloperoxidase‐hydrogen peroxide‐halide system and (3) the D‐amino acid oxidase‐linked system. The S strain was most resistant to all the systems investigated. Synthesis and incorporation of complete S‐like LPS by growing the uridine‐diphosphate‐galactose‐4‐epimeraseless mutant LT2‐M1 in galactose supplemented medium enhanced the resistance to the MPO‐mediated system as the amount of LPS incorporated increased. Among R mutants, bacteria possessing complete or nearly complete basal core LPS (chemotype Ra‐Rb 2 ) were less sensitive to the myeloperoxidase‐mediated system than were mutants more deficient in their cell wall LPS. D‐amino acid oxidase, in combination with D‐alanine and a myeloperoxidase‐containing leucocyte extract, produced a bactericidal system efficient even on the S‐strain. The very deficient Rd mutant R10, but not the S‐strain, was sensitive to the activity of D‐amino acid oxidase even without the addition of D‐amino acids, indicating that the bacteria can serve as an enzyme substrate. These results demonstrate the decisive influence of the bacterial cell surface structure on the efficiency of intracellular bactericidal systems on enterobacteria.