Analyses of Lipopolysaccharides Extracted from Penicillin-Resistant, Serum-Sensitive Salmonella Mutants

Nelson, Brock; Roantree, Robert J.

doi:10.1099/00221287-48-2-179

Cited by 57 publications

(47 citation statements)

References 15 publications

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“…The increase in serum sensitivity that accompanies the loss by mutation of 0 side-chains (DlabaE, 1968) may, therefore, be related to the simulataneous decrease in protein content of the outer membrane (Ames, Spudich and Nikaido, 1974). A small number of serum-sensitive mutants derived from serum-resistant salmonellae by Nelson and Roantree (1967) retained the cultural characteristics of the smooth parent strains and showed unaltered LPS 0-side-chain-sugar to core-sugar ratios.…”

Section: Discussionmentioning

confidence: 99%

“…The yield was expressed as the weight of antigen (mg) per g dry weight of bacterial cells. Phenol-soluble LPS has been found by Hickman and Ashwell (1966) and by Raff and Wheat (1968). Therefore, all phenol layers from phenol-water extractions were examined for LPS.…”

Section: Methodsmentioning

confidence: 99%

“…Studies of resistance to serum have therefore been concerned with cell-surface structures that might impede the attachment or subsequent activity of the serum factors. Mutations leading to reduction or loss of 0 side-chains of LPS result in a marked increase in serum sensitivity (Nelson and Roantree, 1967;DlabaE, 1968;Muschel and Larsen, 1970); it has therefore been suggested that long or numerous 0 side-chains interfere with the functioning of complement and are thus responsible for resistance to serum. Furthermore, phenotypic modification from serum resistance to serum sensitivity is accompanied by a striking reduction in the ratio of 0 side-chain to core sugars (Feingold, 1969).…”

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confidence: 99%

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Immunochemical investigations on lipopolysaccharides and acidic polysaccharides from serum-sensitive and serum-resistant strains of Escherichia coli isolated from urinary-tract infections

Taylor

1976

Journal of Medical Microbiology

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ESCHERICHIA COLI LIPOPOL YSACCHARIDE 407Sensitivity to bacteriophages. Acidic polysaccharides and LPS 0 side-chains are known to interfere with the attachment of rough-specific phages. The phage sensitivity of the bacterial strains was therefore determined with six phages (nos. FO, Br2, BrlO, Fpl, 6SR and C21) which are actively lytic against certain R forms of E. coli (Schmidt et al., 1969). Phages were propagated on suitable host strains and bacterial sensitivity was determined by applying drops of phage containing approximately 108 p.f.u. per ml on to surface-inoculated nutrientagar plates. The phages and their host strains were supplied by Dr G. Schmidt.Preparation of LPS and acidic polysaccharides. The bacteria were grown in 4 x 700-ml amounts of Nutrient Broth (Oxoid no. 2) in 2.5-litre conical flasks. The cultures were incubated in an orbital incubator (120 orbits per min.) at 37°C for 16 h, harvested by centrifugation (O' C), washed twice with 0.4 % NaCl and dried to constant weight over PzOS.Two batches of each strain were prepared. One was extracted with 45 % phenol at 68°C (Westphal and Jann, 1965) and the other with 0.9 % NaCl at 60°C as described by Jann et al.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Immunochemical investigations on lipopolysaccharides and acidic polysaccharides from serum-sensitive and serum-resistant strains of Escherichia coli isolated from urinary-tract infections

Taylor

1976

Journal of Medical Microbiology

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“…Serum-sensitive mutants have been derived from serum-resistant strains by a number of workers (Nelson & Roantree, 1967;Medearis, Camitta & Heath, 1968;Muschel & Larsen, 1970) but, unfortunately, the majority of such mutants are rough or part-rough and differences between these strains cannot be used to explain the behaviour in serum of smooth isolates. An attempt was therefore made to isolate serum-resistant mutants from some of the smooth serum-sensitive E. coli strains considered in a previous study (Taylor, unpublished).…”

Section: Introductionmentioning

confidence: 99%

Genetical Studies of Serum Resistance in Escherichia coli

Taylor¹

1975

Journal of General Microbiology

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One induced and one spontaneous serum-resistant mutant were derived from smooth serum-sensitive Escherichia coli strains. There was little difference in the yield or the 0-side-chain-sugar to core-sugar ratio of lipopolysaccharides from the mutants compared with the parental strains. The mutations to serum resistance were not accompanied by increases in either the amount or haemagglutinationinhibiting activity of acidic polysaccharides extracted from the strains.Two colonially rough forms, designated 17fa and 17gb, were isolated from an aged culture of serum-resistant mutant 17. Escherichia coli 17fa appeared to be a som mutant and was rapidly killed by serum. Escherichia coli 17gb retained serological 0-specificity, and 17gb lipopolysaccharide contained a full complement of 0-side-chains; the strain was killed by serum but only after a delay of I h.Escherichia coli K-negative 0 8 donor Hfryj, which was serum-resistant, was crossed with rough serum-sensitive E. coli strain ~4 7 0 and his+ recombinants were selected. The majority of his+ recombinants inherited a full complement of lipopolysaccharide 0-side-chains but were killed by serum after a delay of I to 2 h.These results suggest that lipopolysaccharide 0-side-chains are responsible for a delay in the killing by normal human serum of smooth E. coli strains but that other factors determine full serum resistance. No evidence was found of a role for K-antigens in serum resistance.

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“…In Salmonella and related genera, rough mutants, of all types tested, are readily killed by exposure to complement-containing normal serum (Nelson & Roantree, 1967), and selection for penicillin-resistance yields mutants some of which are 'rough', as discussed in the Introduction. Thus, the salient features of the phenotype of R146 are all explicable by the postulated partial defect of a transferase function needed for assembly of the 0-repeat unit.…”

Section: Discussionmentioning

confidence: 99%

Mapping of Genes Determining Penicillin-resistance and Serum-sensitivity in Salmonella enteritidis

1980

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Two presumptive single-step mutants, resistant to penicillin and sensitive to the bactericidal effect of normal human serum, were isolated on penicillin gradient plates from a smooth, penicillin-sensitive, serum-resistant strain of Salmonella enteritidis (09,12 ; gal hisEI cys).The chemical composition of their lipopolysaccharides, their phage-sensitivity patterns, and their serological and cultural properties showed one to be 'part-rough' and the other smooth. Hfr strains with 0 antigens 04,5,12 or 01,4,5,12 (two Salmonella typhimurium and one S. abony) and one S. enteritidis F', 09,12, were crossed with the S. enteritidis 09,12 mutants. The results with the part-rough mutant indicate that its penicillin-resistance, serum-sensitivity and rough phage pattern result from a single mutation between hisEI and the part of the rfb gene cluster determining 0 specificity, 4 (abequose) or 9 (tyvelose). Transduction experiments confirmed that the mutation is closely linked to the his operon. This mutation is inferred to cause an incomplete defect in a transferase for galactose, mannose or rhamnose, the smooth sugars common to 04,5,12 and 09,12. Results from similar crosses to the smooth, serum-sensitive, penicillin-resistant S. enteritidis mutant indicate that its serum-sensitivity is not linked to his. The occasional independent segregation of penicillin-resistance and serum-sensitivity suggests that other loci modify penicillinresistance. I N T R O D U C T I O NMichael & Braun (1958) reported that passage of strains of Shigella dysenteriae or Escherichia coli on a series of gradient plates, each with a higher concentration of penicillin than the preceding one, yielded penicillin-resistant mutants which were more easily killed by exposure to normal serum (antibody plus complement) than were the parent strains, but which retained the 0-antigenic specificities of the parent strains. Roantree & Steward (1965) used this method to derive serum-sensitive mutants from serum-resistant, smooth Salmonella enteritidis and Salmonella typhimurium strains, to test whether becoming serum-sensitive reduced virulence. They observed that in a series of mutants, derived stepwise from a given parent strain, only one or a few of the mutations causing increased penicillin-resistance were associated with increased sensitivity to serum. Some serum-sensitive strains were apparently smooth, others were rough, as indicated by colonial morphology and growth with deposit in broth. Nelson & Roantree (1967) characterized lipopolysaccharides (LPS) from these mutants and from single-step penicillin-or cephalothin-resistant mutants of the same two parent strains. The mutants fell into five groups: (a) hapten-negative rough mutants lacking detectable 0-specific material in the LPS and L1 fraction [the supernatant after ultraj-Present address:

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Analyses of Lipopolysaccharides Extracted from Penicillin-Resistant, Serum-Sensitive Salmonella Mutants

Cited by 57 publications

References 15 publications

Immunochemical investigations on lipopolysaccharides and acidic polysaccharides from serum-sensitive and serum-resistant strains of Escherichia coli isolated from urinary-tract infections

Immunochemical investigations on lipopolysaccharides and acidic polysaccharides from serum-sensitive and serum-resistant strains of Escherichia coli isolated from urinary-tract infections

Genetical Studies of Serum Resistance in Escherichia coli

Mapping of Genes Determining Penicillin-resistance and Serum-sensitivity in Salmonella enteritidis

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