MrkD 1P from Klebsiella pneumoniae Strain IA565 Allows for Coexistence with Pseudomonas aeruginosa and Protection from Protease-Mediated Biofilm Detachment
Autor: | Tricia A. Van Laar, Brandon M. Childers, Kai P. Leung, Tao You, Steven Clegg |
---|---|
Rok vydání: | 2013 |
Předmět: |
Proteases
Klebsiella pneumoniae Immunology Mutant Biology medicine.disease_cause Microbiology Bacterial Adhesion medicine Humans Genetic Testing Adhesins Bacterial Gene Library Effector Pseudomonas aeruginosa Wild type Biofilm Bacterial Infections biochemical phenomena metabolism and nutrition biology.organism_classification Culture Media Bacterial adhesin Mutagenesis Insertional Infectious Diseases Biofilms Microbial Interactions Parasitology Fimbriae Proteins Gene Deletion Peptide Hydrolases Plasmids |
Zdroj: | Infection and Immunity. 81:4112-4120 |
ISSN: | 1098-5522 0019-9567 |
Popis: | Biofilm formation and persistence are essential components for the continued survival of pathogens inside the host and constitute a major contributor to the development of chronic wounds with resistance to antimicrobial compounds. Understanding these processes is crucial for control of biofilm-mediated disease. Though chronic wound infections are often polymicrobial in nature, much of the research on chronic wound-related microbes has focused on single-species models. Klebsiella pneumoniae and Pseudomonas aeruginosa are microbes that are often found together in wound isolates and are able to form stable in vitro biofilms, despite the antagonistic nature of P. aeruginosa with other organisms. Mutants of the K. pneumoniae strain IA565 lacking the plasmid-borne mrkD 1P gene were less competitive than the wild type in an in vitro dual-species biofilm model with P. aeruginosa (PAO1). PAO1 spent medium inhibited the formation of biofilm of mrkD 1P -deficient mutants and disrupted preestablished biofilms, with no effect on IA565 and no effect on the growth of the wild type or mutants. A screen using a two-allele PAO1 transposon library identified the LasB elastase as the secreted effector involved in biofilm disruption, and a purified version of the protein produced results similar to those with PAO1 spent medium. Various other proteases had a similar effect, suggesting that the disruption of the mrkD 1P gene causes sensitivity to general proteolytic effects and indicating a role for MrkD 1P in protection against host antibiofilm effectors. Our results suggest that MrkD 1P allows for competition of K. pneumoniae with P. aeruginosa in a mixed-species biofilm and provides defense against microbial and host-derived proteases. |
Databáze: | OpenAIRE |
Externí odkaz: |