Serum Resistance in E.coli

Timmis, Kenneth N.; Manning, Paul A.; Echarti, C.; Timmis, J. K.; Moll, A

doi:10.1007/978-1-4684-3983-0_14

Cited by 24 publications

(19 citation statements)

References 26 publications

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“…These findings support the conclusion that the TraT protein does not actively inhibit phagocytosis, because its inhibitory effect can be overcome by antibodies against either the TraT protein or other surface antigens (29). These results also agree with previous results that indicate that the TraT protein confers upon E. coli serum resistance by a mechanism that does not involve degradation or inactivation of the components of the complement system (47).…”

Section: Methodssupporting

confidence: 93%

“…Ability of the TraT protein to interfere with phagocytosis is independent of the bacterial capsule. Since the bacterial capsule is a surface structure capable of increasing bacterial resistance to serum (2,27,43,47), it was of interest to determine the possible influence of the presence of a bacterial capsule on the inhibition of phagocytosis mediated by the TraT protein. Plasmid pKT107 was therefore introduced by transformation into the capsuleless strain E. coli FC004.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

A plasmid-encoded outer membrane protein, TraT, enhances resistance of Escherichia coli to phagocytosis

Agüero¹,

Aron²,

Am³

et al. 1984

Infect Immun

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The presence of the outer membrane protein TraT, encoded by plasmid R6-5, reduces the sensitivity of Escherichia coli cells to phagocytosis by macrophages. This effect is independent of the bacterial capsule and is more evident in the presence of adsorbed normal human serum. The property of inhibiting phagocytosis is specifically abolished by anti-TraT protein antiserum and anti-TraT immunoglobulin G but not by Fab fragments. These results indicate that the TraT protein is a passive inhibitor of phagocytosis. Inhibition of phagocytosis is produced because the TraT protein antagonizes opsonization by complement, such that C3 deposition is reduced and altered in distribution.Phagocytosis and the bacteriostatic and bactericidal properties of the serum constitute the first line of defense against invasive bacterial infections. The antibacterial activity of blood is effective in eliminating most normally encountered transient bacteremias and is the result of a constellation of specific (e.g., antibodies) and nonspecific (e.g., complement, iron-binding proteins) factors (7,16).The ability of bacteria to avoid host defenses and become invasive rests largely in cell surface components which are important in the preliminary steps of the infective process and crucial in determining its outcome (35). The role of surface components such as capsules, peptidoglycan, proteins, pili, and 0-antigens in increasing the virulence of bacteria is well documented (34). Although most of these are encoded by genetic determinants located on the chromosome, recent reports testify to the importance of plasmidencoded gene product modifications to the cell surface, which alter bacterial virulence (13-15, 31, 33, 34).The Escherichia coli plasmid R6-5 carries a gene specifying resistance to the antibacterial activity of serum (31). This determinant, which has been identified as traT, is one of the genes of the tra operon, the genetic unit conferring conjugative ability upon the bacterial cell (1, 31). The traT gene directs the synthesis of a highly exposed outer membrane protein, which mediates resistance to serum. Since phagocytosis, the other main line of defense against invasive bacterial infections, involves complement, we explored the possibility that the TraT protein may confer upon bacteria the ability to resist phagocytosis. In this communication, we show that this is the case and that the protein interferes mainly with opsonization by the alternative pathway of complement by restricting and altering the pattern of C3 deposition. MATERIALS AND METHODSBacterial strains and plasmids. Bacterial strains and plasmids are listed in Table 1. Plasmid DNA, isolated by standard procedures, was introduced into bacterial strains by transformation or conjugation (45). Strains were stored at -20°C in 60% glycerol. Molecular cloning procedures. Restriction endonuclease * Corresponding author.cleavage of plasmid DNA, ligation reactions, transformations, screening, and analysis by agarose gel electrophoresis were performed as described (45,46). Media. ...

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Section: Methodssupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

A plasmid-encoded outer membrane protein, TraT, enhances resistance of Escherichia coli to phagocytosis

Agüero¹,

Aron²,

Am³

et al. 1984

Infect Immun

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“…Silver et al (1981) cloned the K 1 genes into a K 12 host and found that the recipient K 12 strain expressing the K 1 polysaccharide was resistant to serum 563 564 IDA 0RSKOV AND F. 0RSKOV killing. Timmis et al (1981) found in similar cloning experiments that K 12 recipients of K 1 were resistant to serum killing at low concentrations of serum, but not at higher concentrations. Stevens et al (1978) and Pluschke et al (1983) showed that the sialic acid containing K 1 capsule inhibited the activation of the alternative complement pathway.…”

Section: Bacteraemiamentioning

confidence: 77%

Escherichia coliin extra-intestinal infections

Ørskov

1985

J. Hyg.

220

161

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When Theodor Escherich (1885a, b) first describedEscherichia colihe looked on it as a saprophytic organism. Soon several investigators found that colibacteria could be isolated from intestinal infections and from many infections outside the intestine, like urinary tract infections (UTI), cholecystitis, wound infections, meningitis, septicaemia, pulmonary infections, and many more. Uhlenhuth (1897) showed that coli strains from pathological processes were more pathogenic in animal experiments than strains isolated from the normal intestine. Smith (1927), who examined strains from white scours in calves, showed that spontaneous acapsular mutants could be obtained from certain colibacteria, and that such mutants were less virulent when injected intra-peritoneally into guinea-pigs.

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“…The same host was used in the propagation of the Kl-specific phages (A, B, C, D, and E) which were originally isolated and characterized by Gross et al (4). The procedures for propagation and titration of phages have been previously described fully (24).…”

Section: Methodsmentioning

confidence: 99%

K antigen and serum sensitivity of rough Escherichia coli

Opal¹,

Cross²,

Gemski³

1982

Infect Immun

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We prepared bacterial hybrids which express both Kl and K27 antigens and examined the relative contributions of these capsules to serum resistance. Escherichia coli Hfr strain F639 (rough, K27+, serum sensitive) was conjugated with E. coli recipient strain E412 (rough, Kl+, His-Trp-Strr, serum resistant). Transconjugants which inherited both the his and trp linked genes for K27 antigen synthesis were analyzed. These hybrids retained and expressed the Kl antigen

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Serum Resistance in E.coli

Cited by 24 publications

References 26 publications

A plasmid-encoded outer membrane protein, TraT, enhances resistance of Escherichia coli to phagocytosis

A plasmid-encoded outer membrane protein, TraT, enhances resistance of Escherichia coli to phagocytosis

Escherichia coliin extra-intestinal infections

K antigen and serum sensitivity of rough Escherichia coli

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