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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Functional Insights From KpfR, a New Transcriptional Regulator of Fimbrial Expression That Is Crucial for Klebsiella pneumoniae Pathogenicity

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Author(s):
Inacio Gomes, Ana Erika [1] ; Pacheco, Thaisy [1] ; dos Santos, Cristiane da Silva [1] ; Pereira, Jose Aires [2] ; Ribeiro, Marcelo Lima [3] ; Darrieux, Michelle [1] ; Caldas Ferraz, Lucio Fabio [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Francisco, Lab Biol Mol Microrganismos, Braganca Paulista, SP - Brazil
[2] Univ Sao Francisco, Lab Biol Mol & Celular Tumores, Braganca Paulista, SP - Brazil
[3] Univ Sao Francisco, Lab Imunofarmacol & Biol Mol, Braganca Paulista, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: FRONTIERS IN MICROBIOLOGY; v. 11, JAN 21 2021.
Web of Science Citations: 0
Abstract

Although originally known as an opportunistic pathogen, Klebsiella pneumoniae has been considered a worldwide health threat nowadays due to the emergence of hypervirulent and antibiotic-resistant strains capable of causing severe infections not only on immunocompromised patients but also on healthy individuals. Fimbriae is an essential virulence factor for K. pneumoniae, especially in urinary tract infections (UTIs), because it allows the pathogen to adhere and invade urothelial cells and to form biofilms on biotic and abiotic surfaces. The importance of fimbriae for K. pneumoniae pathogenicity is highlighted by the large number of fimbrial gene clusters on the bacterium genome, which requires a coordinated and finely adjusted system to control the synthesis of these structures. In this work, we describe KpfR as a new transcriptional repressor of fimbrial expression in K. pneumoniae and discuss its role in the bacterium pathogenicity. K. pneumoniae with disrupted kpfR gene exhibited a hyperfimbriated phenotype with enhanced biofilm formation and greater adhesion to and replication within epithelial host cells. Nonetheless, the mutant strain was attenuated for colonization of the bladder in a murine model of urinary tract infection. These results indicate that KpfR is an important transcriptional repressor that, by negatively controlling the expression of fimbriae, prevents K. pneumoniae from having a hyperfimbriated phenotype and from being recognized and eliminated by the host immune system. (AU)

FAPESP's process: 13/13949-9 - Genotypic and phenotypic characterization of Klebsiella pneumoniae isolated from urinary tract infections and in vitro analysis of the processes of host cells adhesion and invasion
Grantee:Thaisy Eliza Pacheco dos Santos
Support type: Scholarships in Brazil - Master
FAPESP's process: 08/11365-1 - Study of the mechanism of gene expression regulation by Fur regulator in Klebsiella pneumoniae: consequences on the expression of virulence factors mediated by quorum-sensing
Grantee:Lúcio Fábio Caldas Ferraz
Support type: Regular Research Grants
FAPESP's process: 18/26203-9 - Study of the contribution of polyamine biosynthesis and transport pathways to the pathogenicity of Klebsiella pneumoniae
Grantee:Lúcio Fábio Caldas Ferraz
Support type: Regular Research Grants
FAPESP's process: 13/06042-7 - In vivo and in vitro studies of the adhesion and invasion of host cells by a fimbriae-deficient mutant strain of Klebsiella pneumoniae
Grantee:Lúcio Fábio Caldas Ferraz
Support type: Regular Research Grants