Cloning of determinants encoding F1652 fimbriae from porcine septicaemic Escherichia coli confirms their identity as F1C fimbriae

Harel, Josée; Jacques, Mario; Fairbrother, John M.; Bossé, Marc; Forget, Céline

doi:10.1099/00221287-141-1-221

Cited by 20 publications

(16 citation statements)

References 41 publications

(19 reference statements)

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“…F1C fimbriae are produced by E. coli causing UTI in humans[16]. In addition F165 2 fimbriae, which are homologous to F1C fimbriae, are expressed by F165‐positive E. coli associated with porcine septicemia and diarrhea [14, 23]. However, it is unknown whether these fimbriae contribute to the pathogenicity of E. coli implicated in either human UTI or porcine extraintestinal or intestinal disease.…”

Section: Resultsmentioning

confidence: 99%

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Dozois

Clément

Désautels

et al. 2006

FEMS Microbiology Letters

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Nineteen papC-positive cytotoxic necrotizing factor 1 (CNF1)-producing Escherichia coli isolates from pigs with septicemia or diarrhea were tested for the presence of pap-, sfa-, and afa-related sequences encoding P/Prs, S/F1C, and Dr/AFA adhesins respectively. Production of adhesins by isolates was tested by mannose-resistant hemagglutination (MRHA), sialidase treatment of erythrocytes and particle agglutination tests. Production of P, S, and F1C fimbriae by isolates was also examined by immunofluorescence. All isolates were pap+ by PCR. Eighteen isolates (95%) were MRHA for ovine and human A erythrocytes and exhibited GalNac-GalNac receptor specificity associated with class III P(Prs) adhesins. Fifteen (79%) of the 19 isolates reacted with antisera specific for one or more different P fimbrial serotypes on immunofluorescence. Three of these isolates also demonstrated Gal-Gal receptor specificity associated with class I or II P fimbrial adhesins. Fifteen (79%) of the isolates were sfa+ by PCR. Seven of these isolates exhibited sialidase-sensitive MRHA of bovine and human O erythrocytes and reacted with serum specific for S fimbriae on immunofluorescence. Seven of the 8 sfa+ isolates which were MRHA-negative for bovine erythrocytes reacted with serum specific for F1C fimbriae on immunofluorescence. All isolates produced type 1 fimbriae as determined by mannose-sensitive agglutination of yeast cells. None of the isolates were afa+ by PCR or colony hybridization. Results suggest that most pap+ porcine CNF1-producing E. coli isolates express P fimbriae bearing class III (Prs) type adhesins. In addition, most of these isolates also produce S or F1C fimbriae.

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Section: Resultsmentioning

confidence: 99%

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Dozois

Clément

Désautels

et al. 2006

FEMS Microbiology Letters

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“…Preparation of fimbrial extracts and Western blotting. Preparation of fimbrial extracts and Western blotting were performed as described previously (20), with anti-FimA serum from E. coli strain B AM and F1C fimbria-specific (anti-F165 2 ) antiserum (35).…”

Section: Methodsmentioning

confidence: 99%

Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

et al. 2012

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The pstSCAB-phoU operon encodes the phosphate-specific transport system (Pst). Loss of Pst constitutively activates the Pho regulon and decreases bacterial virulence. However, specific mechanisms underlying decreased bacterial virulence through inactivation of Pst are poorly understood. In uropathogenic Escherichia coli (UPEC) strain CFT073, inactivation of pst decreased urinary tract colonization in CBA/J mice. The pst mutant was deficient in production of type 1 fimbriae and showed decreased expression of the fimA structural gene which correlated with differential expression of the fimB, fimE, ipuA, and ipbA genes, encoding recombinases, mediating inversion of the fim promoter. The role of fim downregulation in attenuation of the pst mutant was confirmed using a fim phase-locked-on derivative, which demonstrated a significant gain in virulence. In addition, the pst mutant was less able to invade human bladder epithelial cells. Since type 1 fimbriae contribute to UPEC virulence by promoting colonization and invasion of bladder cells, the reduced bladder colonization by the pst mutant is predominantly attributed to downregulation of these fimbriae. Elucidation of mechanisms mediating the control of type 1 fimbriae through activation of the Pho regulon in UPEC may open new avenues for therapeutics or prophylactics against urinary tract infections. Pathogenic Escherichia coli comprises a diversity of strains associated with both intestinal and extraintestinal infections (39). Urinary tract infections (UTIs) are one of the most common bacterial infections, and uropathogenic E. coli (UPEC) is the predominant causal agent, representing up to 85% of communityacquired UTIs (28). In addition to causing UTIs, extraintestinal pathogenic E. coli (ExPEC) is an important pathogen associated with neonatal meningitis and septicemia in humans, as well as systemic infections in poultry and livestock (60, 61). Many virulence factors associated with UPEC strains are important for establishing infection, and these include adhesins, toxins, iron acquisition systems, and capsular antigens (53).An important aspect of bacterial virulence is the capacity to rapidly adapt to changes and stresses encountered during infection of the host, since changes in the host environment may serve as cues mediating regulation of expression of key virulence factors during infection (25,47). One of the mechanisms by which bacteria respond to environmental signals is through two-component signal transduction systems (TCSs). TCSs are composed of an inner-membrane histidine kinase sensor protein and cytoplasmic response regulator (81). TCSs are important for bacterial adaptation and virulence (6, 12), and a number of TCSs have been identified to be important for pathogenic E. coli, e.g., BarA-UvrY, PhoPQ, and QseBC (4, 31, 41, 56).The Pho regulon is controlled by the PhoBR TCS, in which PhoR is the sensor histidine kinase and PhoB the response regulator. PhoBR responds to phosphate limitation, i.e., when the extracellular phosphate concentration falls belo...

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“…The regulatory region of foo shares more than 96% identity with that of the pyelonephritis-associated pili (pap) gene. Previous work showed that F165 1 fimbriae are essential for virulence and survival during systemic stages of infection in young pigs (5)(6)(7)(8). F165 1 fimbriae are principally found in infections caused by opportunistic E. coli in animals, while Pap fimbriae are found in human clinical cases of urinary tract infections.…”

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confidence: 99%

Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

et al. 2015

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A dherence to host cells relies on the synthesis of specialized molecules that play an important role in multiple steps during the infectious process. Adhesins contribute to virulence by promoting the attachment and bacterial colonization on the host cell surface. Escherichia coli possesses a wide variety of adhesins, which all differ in structure and in functions. Moreover, a single strain can present more than one adhesin. This implies a complex regulatory network to produce exclusively one adhesin or to simultaneously express more than one.Phase variation of P fimbriae is a stochastic and reversible switch between an on phenotype and an off phenotype, "all-ornothing" (ON/OFF), each capable of responding to a specific condition. After cell division, the majority of daughter cells retain the expression phase of the parent; a minority switches to the opposite expression phase. F165 1 fimbriae, encoded by the foo gene cluster, are members of the type P fimbria family of Escherichia coli (1-4). The regulatory region of foo shares more than 96% identity with that of the pyelonephritis-associated pili (pap) gene. Previous work showed that F165 1 fimbriae are essential for virulence and survival during systemic stages of infection in young pigs (5-8). F165 1 fimbriae are principally found in infections caused by opportunistic E. coli in animals, while Pap fimbriae are found in human clinical cases of urinary tract infections. The phase variation of F165 1 fimbriae shares similar features with that of the wellcharacterized Pap fimbriae (9-11). This includes an ϳ400-bp intergenic region surrounded by two divergently transcribed genes (papI and papB for Pap, fooI and fooB for F165 1 ). It also includes six leucine-responsive regulatory protein (Lrp) binding sites, of which two are GATC sites (referred to as GATC prox and GATC dist , respectively), spaced 102 bp apart. In pap and foo, phase variation occurs because of methylation-controlled modifications within the regulatory region of the fimbrial operon. This regulation is epigenetic since it does not involve any changes in DNA sequence (12). The differential methylation status of these sequences determines the binding of Lrp. Indeed, the switch from one phenotype to the other arises from the competition between the binding of Lrp at its distal or proximal binding sites and methylation by the Dam methyltransferase at the opposite GATC site (for reviews, see references 9, 10, and 11). When GATC dist is fully methylated, Lrp cooperatively binds to sites 1 to 3, maintaining the cells in the OFF state; when GATC prox is fully methylated, Lrp binds to sites 4 to 6, maintaining the ON state (Fig. 1). Control of pap expression also requires the action of PapI, a positive regulator that increases the affinity of Lrp for sites 4 to 6 in vivo (11,13). PapB, the second specific regulator of the pap operon, plays an important role by coordinating the expression of the pBA and pI promoters (11). All together, the combined actions of Lrp, Dam methyltransferase, PapI, and PapB result...

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Cloning of determinants encoding F1652 fimbriae from porcine septicaemic Escherichia coli confirms their identity as F1C fimbriae

Cited by 20 publications

References 41 publications

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

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Cloning of determinants encoding F1652 fimbriae from porcine septicaemic Escherichia coli confirms their identity as F1C fimbriae

Cited by 20 publications

References 41 publications

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Expression of P, S, and F1C adhesins by cytotoxic necrotizing factor 1-producing Escherichia coli from septicemic and diarrheic pigs

Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

Monitoring F165 1 P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype

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Monitoring F165 ₁ P-Like Fimbria Expression at the Single-Cell Level Reveals a Highly Heterogeneous Phenotype