Nucleotide sequence and functions of mrk determinants necessary for expression of type 3 fimbriae in Klebsiella pneumoniae

Allen, Bradley L.; Gerlach, Gerald-F.; Clegg, Steven

doi:10.1128/jb.173.2.916-920.1991

Cited by 111 publications

(80 citation statements)

References 22 publications

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“…5). MrkB, -C, and -E are involved in assembly and the regulation of expression, while MrkF is involved in the surface stability of the fimbriae (287). In a manner similar to that of type 1 fimbriae, the type 3 fimbria-encoding operon is found in and expressed by almost all K. pneumoniae isolates.…”

Section: Type 1 and 3 Fimbriaementioning

confidence: 96%

Klebsiella pneumoniae: Going on the Offense with a Strong Defense

Paczosa

Mecsas

2016

Microbiol Mol Biol Rev

1,366

1,345

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SUMMARYKlebsiella pneumoniaecauses a wide range of infections, including pneumonias, urinary tract infections, bacteremias, and liver abscesses. Historically,K. pneumoniaehas caused serious infection primarily in immunocompromised individuals, but the recent emergence and spread of hypervirulent strains have broadened the number of people susceptible to infections to include those who are healthy and immunosufficient. Furthermore,K. pneumoniaestrains have become increasingly resistant to antibiotics, rendering infection by these strains very challenging to treat. The emergence of hypervirulent and antibiotic-resistant strains has driven a number of recent studies. Work has described the worldwide spread of one drug-resistant strain and a host defense axis, interleukin-17 (IL-17), that is important for controlling infection. Four factors, capsule, lipopolysaccharide, fimbriae, and siderophores, have been well studied and are important for virulence in at least one infection model. Several other factors have been less well characterized but are also important in at least one infection model. However, there is a significant amount of heterogeneity inK. pneumoniaestrains, and not every factor plays the same critical role in all virulentKlebsiellastrains. Recent studies have identified additionalK. pneumoniaevirulence factors and led to more insights about factors important for the growth of this pathogen at a variety of tissue sites. Many of these genes encode proteins that function in metabolism and the regulation of transcription. However, much work is left to be done in characterizing these newly discovered factors, understanding how infections differ between healthy and immunocompromised patients, and identifying attractive bacterial or host targets for treating these infections.

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Section: Type 1 and 3 Fimbriaementioning

confidence: 96%

Klebsiella pneumoniae: Going on the Offense with a Strong Defense

Paczosa

Mecsas

2016

Microbiol Mol Biol Rev

1,366

1,345

View full text Add to dashboard Cite

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“…In addition to Klebsiella species, type 3 fimbriae are common in Enterobacter, Serratia, Proteus, and Providencia isolates (4). Type 3 fimbriae belong to the chaperone-usher class fimbriae and are encoded by the mrk gene cluster, which includes the mrkA gene encoding the major fimbrial subunit and mrkD encoding the fimbrial adhesin responsible for mannoseresistant Klebsiella-like hemagglutination (1). The MrkD adhesin has been shown to mediate adhesion to collagen structures (51); however, the exact identity of the MrkD receptor remains elusive.…”

mentioning

confidence: 99%

Identification of a Conserved Chromosomal Region Encoding Klebsiella pneumoniae Type 1 and Type 3 Fimbriae and Assessment of the Role of Fimbriae in Pathogenicity

2009

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Type 3 fimbriae are expressed by most clinical Klebsiella pneumoniae isolates and mediate adhesion to host structures in vitro. However, the role of type 3 fimbriae in K. pneumoniae virulence has not been evaluated by use of in vivo infection models. In this study, the type 3 fimbrial gene cluster (mrk) of the clinical isolate C3091 is described in detail. The mrk gene cluster was revealed to be localized in close proximity to the type 1 fimbrial gene cluster. Thus, a 20.4-kb fimbria-encoding region was identified and found to be highly conserved among different K. pneumoniae isolates. Interestingly, a homologue to PecS, known as a global regulator of virulence in Erwinia chrysanthemi, was identified in the fimbria-encoding region. Comparison to the previously characterized plasmid encoded mrk gene cluster revealed significant differences, and it is established here that the putative regulatory gene mrkE is not a part of the chromosomally encoded type 3 fimbrial gene cluster. To evaluate the role of type 3 fimbriae in virulence, a type 3 fimbria mutant and a type 1 and type 3 fimbria double mutant was constructed. Type 3 fimbria expression was found to strongly promote biofilm formation. However, the fimbria mutants were as effective at colonizing the intestine as the wild type, and their virulence was not attenuated in a lung infection model. Also, in a urinary tract infection model, type 3 fimbriae did not influence the virulence, whereas type 1 fimbriae were verified as an essential virulence factor. Thus, type 3 fimbriae were established not to be a virulence factor in uncomplicated K. pneumoniae infections. However, since type 3 fimbriae promote biofilm formation, their role in development of infections in catheterized patients needs to be elucidated.

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“…Its functions include being the principle building block of the fimbrial shaft, biofilm formation and establishment of infection. 11 It is conserved among the majority of enterobacteriaceae and therefore an ideal candidate for vaccine and antibody development. Limited work has been done in this regard and no monoclonal antibodies have been tested for any protective effect until recently.…”

Section: 6mentioning

confidence: 99%