scholarly journals The role of fimbriae and flagella in the colonization, invasion and persistence of Escherichia coli O78[ratio ]K80 in the day-old-chick model

2000 ◽  
Vol 124 (3) ◽  
pp. 351-363 ◽  
Author(s):  
R. M. LA RAGIONE ◽  
A. R. SAYERS ◽  
M. J. WOODWARD
Keyword(s):  
Escherichia Coli ◽  
Wild Type ◽  
Single Strain ◽  
Type 1 Fimbriae ◽  
Invasion Model ◽  
Persistence Model

To understand the role of flagella and fimbriae of Escherichia coli O78[ratio ]K80 in avian colibacillosis, day-old chicks were dosed orally with defined afimbriate and or aflagellate mutants and colonization, invasion and persistence compared with that of the wild-type. In an invasion model, chicks were dosed with 1 × 105 c.f.u. of a single strain and mutants defective for type 1 fimbriae, curli fimbriae or flagella colonized livers by 24 h although the numbers of bacteria present were significantly less than the wild-type. Mutants colonized between 50 and 75% of spleens whereas the wild-type colonized 100% of spleens. Additionally, the numbers of mutant bacteria in colonized spleens were significantly less than the wild-type. Surprisingly, mutants defective for the elaboration of more than one appendage were no more attenuated than single mutants. In a persistence model, chicks were dosed with 1 × 102 c.f.u. of a single strain and mutants defective for type 1 or curli or flagella or any combination thereof persisted as assessed by cloacal swabbing for 5 weeks of the experiment less well than the wild-type. In an additional persistence model, chicks were dosed with 5 × 102 c.f.u. of each of wild-type and one mutant together. All mutants were significantly less persistent than the wild-type (P < 0·001) and one mutant which lacked type 1, curli and flagella, was eliminated within 2 weeks. Analysis of the trends of elimination indicated that flagella contributed to persistence more than curli, which contributed more than type 1 fimbriae. Here was evidence for a major role in colonization, invasion and persistence played by type 1, curli and flagella.

scholarly journals Inactivation of ibeA and ibeT Results in Decreased Expression of Type 1 Fimbriae in Extraintestinal Pathogenic Escherichia coli Strain BEN2908

2008 ◽  
Vol 76 (9) ◽  
pp. 4129-4136 ◽  
Author(s):  
Mélanie A. M. Cortes ◽  
Julien Gibon ◽  
Nathalie K. Chanteloup ◽  
Maryvonne Moulin-Schouleur ◽  
Philippe Gilot ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Wild Type Strain ◽  
Coli Strain ◽  
Wild Type ◽  
Adhesive Properties ◽  
Type 1 Fimbriae ◽  
Pathogenic Escherichia Coli ◽  
Genes Encoding

ABSTRACT IbeA in extraintestinal pathogenic Escherichia coli (ExPEC) strains was previously described for its role in invasion. Here we investigated the role of IbeA and IbeT, encoded by a gene located downstream of ibeA, in the adhesion of the avian ExPEC strain BEN2908 to human brain microvascular endothelial cells (HBMEC). The ΔibeA mutant was less adhesive to HBMEC than the wild-type strain BEN2908 was. Because strain BEN2908 also expresses type 1 fimbriae, we measured the adhesion specifically due to IbeA by comparing the adhesive properties of a Δfim derivative of strain BEN2908 to those of a double Δfim ΔibeA mutant. No differences were observed, indicating that the reduction of adhesion in BEN2908 ΔibeA could be due to a decrease in type 1 fimbria expression. We indeed showed that the decreased adhesion of BEN2908 ΔibeA was correlated with a decrease in type 1 fimbria expression. Accordingly, more bacteria had a fim promoter orientated in the off position in a culture of BEN2908 ΔibeA than in a culture of BEN2908. Expression of fimB and fimE, two genes encoding recombinases participating in controlling the orientation of the fim promoter, was decreased in BEN2908 ΔibeA. A reduction of type 1 fimbria expression due to a preferential orientation of the fim promoter in the off position was also seen in an ibeT mutant of strain BEN2908. We finally suggest a role for IbeA and IbeT in modulating the expression of type 1 fimbriae through an as yet unknown mechanism.

scholarly journals Adhesion of Escherichia Coli to Nanostructured Surfaces and the Role of Type 1 Fimbriae

Nanomaterials ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 2247
Author(s):  
Pawel Kallas ◽  
Håvard J Haugen ◽  
Nikolaj Gadegaard ◽  
John Stormonth-Darling ◽  
Mats Hulander ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Urinary Tract Infections ◽  
Virulence Factor ◽  
Wild Type ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
Tract Infections

Bacterial fimbriae are an important virulence factor mediating adhesion to both biotic and abiotic surfaces and facilitating biofilm formation. The expression of type 1 fimbriae of Escherichia coli is a key virulence factor for urinary tract infections and catheter-associated urinary tract infections, which represent the most common nosocomial infections. New strategies to reduce adhesion of bacteria to surfaces is therefore warranted. The aim of the present study was to investigate how surfaces with different nanotopography-influenced fimbriae-mediated adhesion. Surfaces with three different nanopattern surface coverages made in polycarbonate were fabricated by injection molding from electron beam lithography nanopatterned templates. The surfaces were constructed with features of approximately 40 nm width and 25 nm height with 100 nm, 250 nm, and 500 nm interspace distance, respectively. The role of fimbriae type 1-mediated adhesion was investigated using the E. coli wild type BW25113 and ΔfimA (with a knockout of major pilus protein FimA) and ΔfimH (with a knockout of minor protein FimH) mutants. For the surfaces with nanotopography, all strains adhered least to areas with the largest interpillar distance (500 nm). For the E. coli wild type, no difference in adhesion between surfaces without pillars and the largest interpillar distance was observed. For the deletion mutants, increased adhesion was observed for surfaces without pillars compared to surfaces with the largest interpillar distance. The presence of a fully functional type 1 fimbria decreased the bacterial adhesion to the nanopatterned surfaces in comparison to the mutants.

scholarly journals Escherichia coli type-1 fimbriae are critical to overcome initial bottlenecks of infection upon low-dose inoculation in a porcine model of cystitis

Microbiology ◽  
2021 ◽  
Vol 167 (10) ◽  
Author(s):  
Kristian Stærk ◽  
Rasmus Birkholm Grønnemose ◽  
Thomas Kastberg Nielsen ◽  
Nicky Anúel Petersen ◽  
Yaseelan Palarasah ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Porcine Model ◽  
Post Inoculation ◽  
Upec Strain ◽  
Content Type ◽  
Type 1 Fimbriae ◽  
Susceptibility To Infection ◽  
General Importance

Most uropathogenic Escherichia coli (UPEC) express type-1 fimbriae (T1F), a key virulence factor for urinary tract infection (UTI) in mice. Evidence that conclusively associates this pilus with uropathogenesis in humans has, however, been difficult to obtain. We used an experimental porcine model of cystitis to assess the role of T1F in larger mammals more closely related to humans. Thirty-one pigs were infected with UPEC strain UTI89 or its T1F deficient mutant, UTI89ΔfimH, at inoculum titres of 102 to 108 colony forming units per millilitre. Urine and blood samples were collected and analysed 7 and 14 days post-inoculation, and whole bladders were removed at day 14 and analysed for uroepithelium-associated UPEC. All animals were consistently infected and reached high urine titres independent of inoculum titre. UTI89ΔfimH successfully colonized the bladders of 1/6 pigs compared to 6/6 for the wild-type strain. Intracellular UPEC were detectable in low numbers in whole bladder explants. In conclusion, low doses of UPEC are able to establish robust infections in pigs, similar to what is presumed in humans. T1F are critical for UPEC to surpass initial bottlenecks during infection but may be dispensable once infection is established. While supporting the conclusions from mice studies regarding a general importance of T1F in successfully infecting the host, the porcine UTI models’ natural high, more human-like, susceptibility to infection, allowed us to demonstrate a pivotal role of T1F in initial establishment of infection upon a realistic low-inoculum introduction of UPEC in the bladder.

scholarly journals Mutation of the Gene Encoding Cytotoxic Necrotizing Factor Type 1 (cnf1) Attenuates the Virulence of Uropathogenic Escherichia coli

2001 ◽  
Vol 69 (6) ◽  
pp. 3954-3964 ◽  
Author(s):  
Karen E. Rippere-Lampe ◽  
Alison D. O'Brien ◽  
Richard Conran ◽  
Hank A. Lockman
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Human Neutrophils ◽  
Wild Type ◽  
Single Strain ◽  
E Coli ◽  
Cytotoxic Necrotizing Factor ◽  
Positive Strain ◽  
Factor Type

ABSTRACT Cytotoxic necrotizing factor type 1 (CNF1) is a 115-kDa toxin that activates Rho GTPases and is produced by uropathogenicEscherichia coli (UPEC). While both epidemiological studies that link CNF1 production by E. coli with urinary tract disease and the cytopathic effects of CNF1 on cultured urinary tract cells are suggestive of a role for the toxin as a UPEC virulence factor, few in vivo studies to test this possibility have been reported. Therefore, in this investigation, we evaluated the importance of CNF1 in a murine model of urinary tract infection (UTI) by comparing the degree of colonization and damage induced by three different CNF1-producing E. coli strains with isogenic CNF1-deficient derivatives. The data from single-strain challenge experiments with C3H/HeOuJ mice indicated a trend toward higher counts of the wild-type strains in the urine and bladders of these animals up to 3 days after challenge in two of three strain pairs. Furthermore, this difference was statistically significant at day 2 of infection with one strain pair, C189 and C189cnf 1. To control for the animal-to-animal variability inherent in this model, we infected C3H/HeOuJ mice with a mixture of CNF1-positive and -negative isogenic derivatives of CP9. The CNF1-positive strain was recovered in higher numbers than the CNF1-negative strain in the urine, bladders, and kidneys of the mice up to 9 days postinfection. These striking coinfection findings, taken with the trends observed in single-strain infections, led us to conclude that CNF1-negative strains were generally attenuated compared to the wild type in the C3H/HeOuJ mouse model of UTI. Furthermore, histopathological examination of bladder specimens from mice infected with CNF1-positive strains consistently showed deeper, more extensive inflammation than in those infected with the isogenic mutants. Lastly, we found that CNF1-positive strain CP9 was better able to resist killing by fresh human neutrophils than were CP9cnf 1 bacteria. From these data in aggregate, we propose that CNF1 production increases the capacity of UPEC strains to resist killing by neutrophils, which in turn permits these bacteria to gain access to deeper tissue and persist better in the lower urinary tract.

scholarly journals Surface Interactions between Escherichia coli and Hemocytes of the Mediterranean Mussel Mytilus galloprovincialis Lam. Leading to Efficient Bacterial Clearance

2001 ◽  
Vol 67 (1) ◽  
pp. 464-468 ◽  
Author(s):  
Laura Canesi ◽  
Carla Pruzzo ◽  
Renato Tarsi ◽  
Gabriella Gallo
Keyword(s):  
Escherichia Coli ◽  
Mytilus Galloprovincialis ◽  
Inhibitory Effect ◽  
Culturable Bacteria ◽  
Adhesive Properties ◽  
Type 1 Fimbriae ◽  
In Vivo Experiments

ABSTRACT The role of type 1 fimbriae in the interactions betweenEscherichia coli and Mytilus galloprovincialisLam. hemocytes was evaluated. The association of fimbriated strain MG155 with hemocyte monolayers at 18°C was 1.5- and 3- to 4-fold greater than the association of unfimbriated mutant AAEC072 in artificial seawater and in hemolymph serum, respectively. Such differences were apparently due to different adhesive properties since MG155 adhered more efficiently than AAEC072 when hemocytes were incubated at 4°C to inhibit the internalization process. Hemolymph serum increased both association and adherence of MG155 two- to threefold but did not affect association and adherence of AAEC072. MG155 was also 1.5- to 1.7-fold more sensitive to killing by hemocytes than AAEC072, as evaluated by the number of culturable bacteria after 60 and 120 min of incubation. The role of type 1 fimbriae in MG155 interactions with hemocytes was confirmed by the inhibitory effect ofd-mannose. In in vivo experiments MG155 cells were cleared from circulating hemolymph more rapidly than AAEC072 cells were cleared. These results confirm that surface properties are crucial in influencing bacterial persistence and survival within mussel hemolymph.

scholarly journals Role of Avian Pathogenic Escherichia coli Virulence Factors in Bacterial Interaction with Chicken Heterophils and Macrophages

2003 ◽  
Vol 71 (1) ◽  
pp. 494-503 ◽  
Author(s):  
Melha Mellata ◽  
Maryvonne Dho-Moulin ◽  
Charles M. Dozois ◽  
Roy Curtiss ◽  
Brigitte Lehoux ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Virulence Factors ◽  
Primary Cultures ◽  
Temperature Sensitive ◽  
Type 1 Fimbriae ◽  
Bacterial Interaction ◽  
K1 Capsule ◽  
Bacterial Association

ABSTRACT Avian pathogenic Escherichia coli (APEC) cause extraintestinal disease in avian species via respiratory tract infection. Virulence factors associated with APEC include type 1 and P fimbriae, curli, aerobactin, lipopolysaccharide (LPS), K1 capsular antigen, temperature-sensitive hemagglutinin (Tsh), and an uncharacterized pathogen-specific chromosomal region (the 0-min region). The role of these virulence factors in bacterial interaction with phagocytes was investigated by using mutants of three APEC strains, each belonging to one of the most predominant serogroups O1, O2, and O78. Bacterial cell interaction with avian phagocytes was tested with primary cultures of chicken heterophils and macrophages. The presence of type 1 fimbriae and, in contrast, the absence of P fimbriae, K1 capsule, O78 antigen, and the 0-min region promoted bacterial association with chicken heterophils and macrophages. The presence of type 1 and P fimbriae, O78 antigen, and the 0-min region seemed to protect bacteria against the bactericidal effect of phagocytes, especially heterophils. The tested virulence factors seemed to have a limited role in intracellular survival for up to 48 h in macrophages. Generally, opsonized and nonopsonized bacteria were eliminated to the same extent, but in some cases, unopsonized bacteria were eliminated to a greater extent than opsonized bacteria. These results confirm the important role of type 1 fimbriae in promotion of initial phagocytosis, but nevertheless indicate a role for type 1 fimbriae in the protection of bacteria from subsequent killing, at least in heterophils. The results also indicate a role for K1 capsule, O78 antigen, P fimbriae, and the 0-min region in initial avoidance of phagocytosis, but demonstrate an additional role for O78 antigen, P fimbriae, and the 0-min region in subsequent protection against the bactericidal effects of phagocytes after bacterial association has occurred.

scholarly journals Coordinate Expression of Fimbriae in Uropathogenic Escherichia coli

2005 ◽  
Vol 73 (11) ◽  
pp. 7588-7596 ◽  
Author(s):  
Jennifer A. Snyder ◽  
Brian J. Haugen ◽  
C. Virginia Lockatell ◽  
Nathalie Maroncle ◽  
Erin C. Hagan ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Gene Clusters ◽  
Phase Variable ◽  
Type 1 Fimbriae ◽  
Coordinated Expression ◽  
Tract Infections

ABSTRACT Uropathogenic Escherichia coli is the most common etiological agent of urinary tract infections. Bacteria can often express multiple adhesins during infection in order to favor attachment to specific niches within the urinary tract. We have recently demonstrated that type 1 fimbria, a phase-variable virulence factor involved in adherence, was the most highly expressed adhesin during urinary tract infection. Here, we examine whether the expression of type 1 fimbriae can affect the expression of other adhesins. Type 1 fimbrial phase-locked mutants of E. coli strain CFT073, which harbors genes for numerous adhesins, were employed in this study. CFT073-specific DNA microarray analysis of these strains demonstrates that the expression of type 1 fimbriae coordinately affects the expression of P fimbriae in an inverse manner. This represents evidence for direct communication between genes relating to pathogenesis, perhaps to aid the sequential occupation of different urinary tract tissues. While the role of type 1 fimbriae during infection has been clear, the role of P fimbriae must be further defined to assert the relevance of coordinated regulation in vivo. Therefore, we examined the ability of P fimbrial isogenic mutants, constructed in a type 1 fimbrial-negative background, to compete in the murine urinary tract over a period of 168 h. No differences in the colonization of these mutants were observed. However, comparison of these results with previous studies suggests that inversely coordinated expression of adhesin gene clusters does occur in vivo. Interestingly, the mutant that was incapable of expressing either type 1 or P fimbriae compensated by synthesizing F1C fimbriae.

scholarly journals Reciprocal Packaging of the Main Structural Proteins of Type 1 Fimbriae and Flagella in the Outer Membrane Vesicles of “Wild Type” Escherichia coli Strains

2021 ◽  
Vol 12 ◽  
Author(s):  
Sarah A. Blackburn ◽  
Mark Shepherd ◽  
Gary K. Robinson
Keyword(s):  
Escherichia Coli ◽  
Outer Membrane ◽  
Membrane Vesicle ◽  
Outer Membrane Vesicles ◽  
Wild Type ◽  
Protein Fusion ◽  
E Coli ◽  
Type 1 Fimbriae ◽  
K 12

Fundamental aspects of outer membrane vesicle (OMV) biogenesis and the engineering of producer strains have been major research foci for many in recent years. The focus of this study was OMV production in a variety of Escherichia coli strains including wild type (WT) (K12 and BW25113), mutants (from the Keio collection) and proprietary [BL21 and BL21 (DE3)] strains. The present study investigated the proteome and prospective mechanism that underpinned the key finding that the dominant protein present in E. coli K-12 WT OMVs was fimbrial protein monomer (FimA) (a polymerizable protein which is the key structural monomer from which Type 1 fimbriae are made). However, mutations in genes involved in fimbriae biosynthesis (ΔfimA, B, C, and F) resulted in the packaging of flagella protein monomer (FliC) (the major structural protein of flagella) into OMVs instead of FimA. Other mutations (ΔfimE, G, H, I, and ΔlrhA–a transcriptional regulator of fimbriation and flagella biosynthesis) lead to the packaging of both FimA and Flagellin into the OMVs. In the majority of instances shown within this research, the production of OMVs is considered in K-12 WT strains where structural appendages including fimbriae or flagella are temporally co-expressed throughout the growth curve as shown previously in the literature. The hypothesis, proposed and supported within the present paper, is that the vesicular packaging of the major FimA is reciprocally regulated with the major FliC in E. coli K-12 OMVs but this is abrogated in a range of mutated, non-WT E. coli strains. We also demonstrate, that a protein of interest (GFP) can be targeted to OMVs in an E. coli K-12 strain by protein fusion with FimA and that this causes normal packaging to be disrupted. The findings and underlying implications for host interactions and use in biotechnology are discussed.

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