Horizontal gene transfer of the <i>Escherichia coli pap</i> and <i>prs</i> pili operons as a mechanism for the development of tissue‐specific adhesive properties

Marklund, Britt-Inger; Tennent, Jan M.; Garcia, Elisa; Hamers, Anja M.; Båga, Monica; Lindberg, Frederik P.; Gaastra, Wim; Normark, S

doi:10.1111/j.1365-2958.1992.tb01399.x

Cited by 200 publications

(157 citation statements)

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“…There was significant positive correlation between the level of MRHA and the number of P clusters for the isolates, Pearson correlation (r 2 ) of 0?321, P=0?023, showing that those isolates with more P clusters tended to show an increased level of MRHA, as expected from other studies (Blanco et al, 1997;Hull et al, 1994). It should be noted that although the use of human RBCs alone limits recognition to functional expression of PapG class II, since PapG class III binds preferentially to the Forssman antigen present in other species (Marklund et al, 1992), the majority of isolates were positive for agglutination, so MRHA with human RBCs was judged to be sufficient for the purposes of this study. The fact that the pyelonephritis and cystitis groups were more likely to carry a greater number of P clusters than asymptomatic groups and to express P fimbriae increased the probability of papB expression in each cell.…”

supporting

confidence: 50%

“…Single-copy fusions were as follows: egfp was amplified from peGFP using primers GFP 59 and GFP 39 (Roe et al, 2003) and cloned into pAJR25, forming pAJR28, and into pKC8, forming pKC12. pap DNA from strains DL2121, DL 2496 (Nou et al, 1995) and J96 (Hull et al, 1981;Marklund et al, 1992) which included papI ORF, papB ORF and the start codon of papA was amplified with the primers 177P and 178P (Table 4), cloned initially into pCR4TOPO-TA, then subcloned with BamHI and KpnI sites into either pAJR28 or pKC12, for exchange into E. coli K-12 or CFT073 backgrounds, respectively, as described previously Porter et al, 2004). The plasmids constructed corresponded to the mutated pap regulatory regions as follows: pNJH83 (K-12) and pNJH86 (CFT073) contained PpapBA ON from DL 2121, forming ZAP986 and ZAP989; pNJH84 (K-12) and pNJH87 (CFT073) contained PpapBA OFF from DL 2496, forming ZAP987 and ZAP990; pNJH85 (K-12) and pNJH88 (CFT073) contained wild-type PpapBA (J96), forming ZAP988 and ZAP991.…”

Section: Methodsmentioning

confidence: 99%

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Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

et al. 2006

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The majority of Escherichia coli strains isolated from urinary tract infections have the potential to express multiple fimbriae. Two of the most common fimbrial adhesins are type 1 fimbriae and pyelonephritis-associated pili (Pap). Previous research has shown that induced, plasmid-based expression of a Pap regulator, papB, and its close homologues can prevent inversion of the fim switch controlling the expression of type 1 fimbriae. The aim of the present study was to determine if this cross-regulation occurs when PapB is expressed from its native promoter in the chromosome of E. coli K-12 and clinical isolates. The regulation was examined in three ways: (1) mutated alleles of the pap regulatory region, including papB and papI, that maintain the pap promoter in either the off or the on phase were exchanged into the chromosome of both E. coli K-12 and the clinical isolate E. coli CFT073, and the effect on type 1 fimbrial expression was measured; (2) type 1 fimbrial expression was determined using a novel fimS : : gfp + reporter system in mutants of the clinical isolate E. coli 536 in which combinations of complete fimbrial clusters had been deleted; (3) type 1 fimbrial expression was determined in a range of clinical isolates and compared with both the number of P clusters and their expression. All three approaches demonstrated that P expression represses type 1 fimbrial expression. Using a number of novel genetic approaches, this work extends the initial finding that PapB inhibits FimB recombination to the impact of this regulation in clinical isolates. INTRODUCTIONUrinary tract infections (UTIs) are common, affecting a large proportion of the population. It is estimated that 20 % of women develop a UTI in their lifetime, and antibiotic treatment results in approximately 110 000 prescriptions per million inhabitants per annum in Europe (Naber, 2000). Escherichia coli strains are the predominant cause of uncomplicated UTIs, responsible for between 60 and 80 % of the cases reported in the UK each year (Graham & Galloway, 2001). Many infections are asymptomatic, especially in the elderly (Nicolle, 2001), but others result in cystitis. If the infection ascends to the kidney, then pyelonephritis can occur. Such infections are a significant origin of Gramnegative sepsis.Fimbrial adhesins are important virulence factors that allow binding of the bacteria to specific receptors on epithelial cells of the urinary tract. The two adhesins most commonly associated with UTI are type 1 fimbriae, and pyelonephritisassociated pili (Pap) and Pap-related fimbriae (Prf); the last two are collectively termed P fimbriae in this study. Type 1 fimbriae mediate binding to a-D-mannose-containing receptors and extracellular matrix components, whereas P fimbriae bind to glycoreceptors containing the aGal(1-4)bGal moiety (Lindberg et al., 1984). Although type 1 fimbriae are common to the majority of E. coli isolates, the FimH adhesin has been shown to be important in a mouse model of UTI, and a degranulation response to the fimbriae is asso...

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supporting

confidence: 50%

Section: Methodsmentioning

confidence: 99%

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

et al. 2006

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“…Interestingly, an IS element has also been identified at the 39-end of the related sfp operon (Brunder et al, 2001), which might indicate the presence of a PAI. This might even suggest a distribution of these related genes by horizontal gene transfer as had been reported for pap and prs operons (Marklund et al, 1992).…”

Section: Discussionmentioning

confidence: 91%

The Pix pilus adhesin of the uropathogenic Escherichia coli strain X2194 (O2 : K− : H6) is related to Pap pili but exhibits a truncated regulatory region

et al. 2003

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Adhesins provide a major advantage for uropathogenic Escherichia coli in establishing urinary tract infections (UTIs). A novel gene cluster responsible for the expression of a filamentous adhesin of the pyelonephritogenic E. coli strain X2194 has been identified, molecularly cloned, and characterized. The ‘pix operon’ contains eight open reading frames which exhibit significant sequence homology to corresponding genes in the pap operon encoding P pili, the prevalent E. coli adhesins in non-obstructive acute pyelonephritis in humans. Although a pixB gene corresponding to the PapB regulator was identified, a papI homologue could not be found in the pix operon. Instead, a fragment of the R6 gene of the highly uropathogenic E. coli strain CFT073 was identified upstream of pixB. The R6 gene is located in a pathogenicity island containing several pilus-encoding sequences and shows homology to a transposase of Chelatobacter heintzii. In a pixA–lacZ fusion system it was demonstrated that the expression of Pix pili is regulated at the transcriptional level by the R6 gene sequence. A significantly reduced transcription was observed by deleting this fragment and by lowering the growth temperature from 37 to 26 °C. In contrast to other filamentous adhesin systems, Pix pili are mainly expressed in the steady state growth phase and were not repressed by the addition of glucose.

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“…It was reported later that these urinary and faecal isolates expressed similar P-®mbrial adhesins [3], which are the major virulence factors of uropathogenic E. coli. The production of these adhesins is encoded by papG genes [4]. This study investigated whether E. coli isolates from blood, urine and faeces of the same child with urosepsis were genetically identical, as no such study analysing isolates from these three sources with new molecular methods has yet been published.…”

Section: Introductionmentioning

confidence: 99%

Genomic identity of pyelonephritogenic Escherichia coli isolated from blood, urine and faeces of children with urosepsis

Jantunen

Saxén

Lukinmaa

et al. 2001

Journal of Medical Microbiology

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Chromosomal genotypes of Escherichia coli isolates from blood, urine and faeces of infants with urosepsis were studied to ®nd possible clonality of the isolates. The isolates were analysed by PCR for class I, II and III alleles of the pyelonephritis-associated adhesin gene papG. The macrorestriction pro®les of the papG-positive isolates were analysed by pulsed-®eld gel electrophoresis and their O serogroups were determined. Genetically identical E. coli isolates from the blood, urine and faeces of the same infant were found in 8 of 10 infants. This ®nding con®rmed the results of previous phenotypic studies that the reservoir of pyelonephritogenic E. coli is indeed the colon.

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Horizontal gene transfer of the Escherichia coli pap and prs pili operons as a mechanism for the development of tissue‐specific adhesive properties

Cited by 200 publications

References 68 publications

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

Demonstration of regulatory cross-talk between P fimbriae and type 1 fimbriae in uropathogenic Escherichia coli

The Pix pilus adhesin of the uropathogenic Escherichia coli strain X2194 (O2 : K− : H6) is related to Pap pili but exhibits a truncated regulatory region

Genomic identity of pyelonephritogenic Escherichia coli isolated from blood, urine and faeces of children with urosepsis

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