toxigenic strains represent a critical health threat, mainly due to their link to antibiotic-associated hemorrhagic colitis. This serious condition results from the bacteria's ability to produce tilimycin and tilivalline cytotoxins. Our research highlights the pivotal role of OmpR, a key regulator within the EnvZ/OmpR two-component system, in controlling the virulence factors associated with . Our findings strongly indicate that OmpR is a repressor of the and genes, the first genes of and NRPS operons, respectively, which are indispensable for producing these enterotoxins. Notably, in the absence of OmpR, we observe a significant increase in cytotoxic effects on Caco-2 cells. These observations identify OmpR as a crucial negative transcription regulator for both operons, effectively managing the release of these cytotoxins. This research deepens our understanding of the mechanisms of toxigenic and opens promising avenues for targeting OmpR for new therapeutic interventions. By focusing on this innovative approach, we can develop more effective solutions to combat this pressing health challenge, ultimately improving patient outcomes against this pathogen.
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http://dx.doi.org/10.3390/microorganisms13010158 | DOI Listing |
Microorganisms
January 2025
Unidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, Hospital de Pediatría, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City 06720, Mexico.
toxigenic strains represent a critical health threat, mainly due to their link to antibiotic-associated hemorrhagic colitis. This serious condition results from the bacteria's ability to produce tilimycin and tilivalline cytotoxins. Our research highlights the pivotal role of OmpR, a key regulator within the EnvZ/OmpR two-component system, in controlling the virulence factors associated with .
View Article and Find Full Text PDFmSphere
December 2024
Unidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, Mexico.
The toxigenic strains secrete tilymicin and tilivalline enterotoxins, which cause antibiotic-associated hemorrhagic colitis. Both enterotoxins are non-ribosomal peptides synthesized by enzymes encoded in two divergent operons clustered in a pathogenicity island. The transcriptional regulator Lrp (eucine-responsive egulatory rotein) controls the expression of several bacterial genes involved in virulence.
View Article and Find Full Text PDFGut Microbes
November 2024
Institute of Molecular Biosciences, University of Graz, Graz, Austria.
The human intestinal tract is densely colonized by a microbial community that is subject to intense competition. Bacteria in this complex habitat seek to outcompete their neighbors for nutrients and eliminate competitors with antibacterial toxins. Antagonism can be mediated by diverse effectors including toxic proteins and small molecule inhibitors that are released extracellularly or delivered by specialized secretion systems to targeted cells.
View Article and Find Full Text PDFNat Microbiol
July 2024
Department of Microbial Immune Regulation, Helmholtz Center for Infection Research, Braunschweig, Germany.
The Klebsiella oxytoca species complex is part of the human microbiome, especially during infancy and childhood. K. oxytoca species complex strains can produce enterotoxins, namely, tilimycin and tilivalline, while also contributing to colonization resistance (CR).
View Article and Find Full Text PDFmBio
February 2022
Department of Pediatrics, UConn Health, Farmington, Connecticut, USA.
Gastrointestinal microbes respond to biochemical metabolites that coordinate their behaviors. Here, we demonstrate that bacterial indole functions as a multifactorial mitigator of Klebsiella grimontii and Klebsiella oxytoca pathogenicity. These closely related microbes produce the enterotoxins tilimycin and tilivalline; cytotoxin-producing strains are the causative agent of antibiotic-associated hemorrhagic colitis and have been associated with necrotizing enterocolitis of premature infants.
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