Expression of capsular polysaccacharide determines serum resistance in Escherichia coli k92

Suerbaum, Sebastian; Friedrich, Susanne; Leying, Hermann; Opferkuch, W.

doi:10.1016/s0934-8840(11)80565-7

Cited by 9 publications

(7 citation statements)

References 28 publications

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“…To date, the exact mechanism underlying bacterial serum resistance is unknown. Aside from various proteins of the outer membrane, such as the TraT lipoprotein or porins (3,155), primarily CPS and O antigens (lipopolysaccharides [LPS]) have been implicated (49,173,194,230,237,246,252). For Klebsiella, two hypotheses have been propounded (145).…”

Section: Serum Resistance and Lipopolysaccharidementioning

confidence: 99%

Klebsiellaspp. as Nosocomial Pathogens: Epidemiology, Taxonomy, Typing Methods, and Pathogenicity Factors

1998

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SUMMARY Bacteria belonging to the genus Klebsiella frequently cause human nosocomial infections. In particular, the medically most important Klebsiella species, Klebsiella pneumoniae, accounts for a significant proportion of hospital-acquired urinary tract infections, pneumonia, septicemias, and soft tissue infections. The principal pathogenic reservoirs for transmission of Klebsiella are the gastrointestinal tract and the hands of hospital personnel. Because of their ability to spread rapidly in the hospital environment, these bacteria tend to cause nosocomial outbreaks. Hospital outbreaks of multidrug-resistant Klebsiella spp., especially those in neonatal wards, are often caused by new types of strains, the so-called extended-spectrum-β-lactamase (ESBL) producers. The incidence of ESBL-producing strains among clinical Klebsiella isolates has been steadily increasing over the past years. The resulting limitations on the therapeutic options demand new measures for the management of Klebsiella hospital infections. While the different typing methods are useful epidemiological tools for infection control, recent findings about Klebsiella virulence factors have provided new insights into the pathogenic strategies of these bacteria. Klebsiella pathogenicity factors such as capsules or lipopolysaccharides are presently considered to be promising candidates for vaccination efforts that may serve as immunological infection control measures.

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Section: Serum Resistance and Lipopolysaccharidementioning

confidence: 99%

Klebsiellaspp. as Nosocomial Pathogens: Epidemiology, Taxonomy, Typing Methods, and Pathogenicity Factors

1998

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“…Indeed, serum resistance has been shown to be an important virulence trait of APEC (37). Previous studies have shown that many bacterial traits contribute to E. coli's serum resistance, including production of a capsule, a smooth lipopolysaccharide (LPS) layer, and certain outer membrane proteins (OMPs) (37,55), including OmpA, TraT, and Iss (11,40,42,59). OmpA is a major protein in E. coli's outer membrane, TraT is encoded by conjugative F plasmids, and Iss is homologous to the Bor protein of bacteriophage , which is typically encoded by large virulence plasmids in APEC (29).…”

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confidence: 99%

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

Tivendale

Liu

et al. 2011

Infect Immun

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Infections of avian pathogenic Escherichia coli (APEC) result in annual multimillion-dollar losses to the poultry industry. Despite this, little is known about the mechanisms by which APEC survives and grows in the bloodstream. Thus, the aim of this study was to identify molecular mechanisms enabling APEC to survive and grow in this critical host environment. To do so, we compared the transcriptome of APEC O1 during growth in Luria-Bertani broth and chicken serum. Several categories of genes, predicted to contribute to adaptation and growth in the avian host, were identified. These included several known virulence genes and genes involved in adaptive metabolism, protein transport, biosynthesis pathways, stress resistance, and virulence regulation. Several genes with unknown function, which were localized to pathogenicity islands or APEC O1's large virulence plasmid, pAPEC-O1-ColBM, were also identified, suggesting that they too contribute to survival in serum. The significantly upregulated genes dnaK, dnaJ, phoP, and ybtA were subsequently subjected to mutational analysis to confirm their role in conferring a competitive advantage during infection. This genome-wide analysis provides novel insight into processes that are important to the pathogenesis of APEC O1.

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“…Among at least 77 K serotypes distinguished (18), K. pneumoniae strains belonging to serotypes K1 and K2 are the most virulent to mice (17). It has been well documented that CPS protects K. pneumoniae from complement-mediated serum killing and phagocytosis (6,11,30,37).…”

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confidence: 99%

RmpA2, an Activator of Capsule Biosynthesis inKlebsiella pneumoniaeCG43, Regulates K2cpsGene Expression at the Transcriptional Level

2003

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The rmpA2 gene, which encodes an activator for capsular polysaccharide (CPS) synthesis, was isolated from a 200-kb virulence plasmid of Klebsiella pneumoniae CG43. Based on the sequence homology with LuxR at the carboxyl-terminal DNA-binding motif, we hypothesized that RmpA2 exerts its effect by activating the expression of cps genes that are responsible for CPS biosynthesis. Two luxAB transcriptional fusions, each containing a putative promoter region of the K. pneumoniae K2 cps genes, were constructed and were found to be activated in the presence of multicopy rmpA2. The activation is likely due to direct binding of RmpA2 to the cps gene promoter through its C-terminal DNA binding motif. Moreover, the loss of colony mucoidy in a K. pneumoniae strain deficient in RcsB, a regulator for cps gene expression, could be recovered by complementing the strain with a multicopy plasmid carrying rmpA2. The CPS production in Lon protease-deficient K. pneumoniae significantly increased, and the effect was accompanied by an increase of RmpA2 stability. The expression of the rmpA2 gene was negatively autoregulated and could be activated when the organism was grown in M9 minimal medium. An IS3 element located upstream of the rmpA2 was required for the full activation of the rmpA2 promoter. In summary, our results suggest that the enhancement of K2 CPS synthesis in K. pneumoniae CG43 by RmpA2 can be attributed to its transcriptional activation of K2 cps genes, and the expression level of rmpA2 is autoregulated and under the control of Lon protease.

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Expression of capsular polysaccacharide determines serum resistance in Escherichia coli k92

Cited by 9 publications

References 28 publications

Klebsiellaspp. as Nosocomial Pathogens: Epidemiology, Taxonomy, Typing Methods, and Pathogenicity Factors

Klebsiellaspp. as Nosocomial Pathogens: Epidemiology, Taxonomy, Typing Methods, and Pathogenicity Factors

Transcriptome Analysis of Avian Pathogenic Escherichia coli O1 in Chicken Serum Reveals Adaptive Responses to Systemic Infection

RmpA2, an Activator of Capsule Biosynthesis inKlebsiella pneumoniaeCG43, Regulates K2cpsGene Expression at the Transcriptional Level

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