Abstract

The bacteria Burkholderia cenocepacia, which cause pulmonary infections in people with low immunity and in children with inherited diseases such as cystic fibrosis, were studied. The virulence of these bacteria is related with their ability to form viscous biofilms in the lung bronchi and alveoli of patients. Data on the possibility of producing mutants with an altered changed biofilm formation ability using insertion mutagenesis and their characteristics in vivo and in vitro are presented. Three genes involved in the genetic regulation of biofilm formation were identified by cloning and sequencing fragments of mutant genes. Two of the identified genes are the global regulatory genes ompR and tetR, and their mutations result in a decrease or higher ability to form biofilms of B. cenocepacia. Proteomic analysis identified the proteins in mutant strains with a different expression level than in the initial strains. The adhesive properties of the biofilms formed by initial and mutant strains of Burkholderia were evaluated using light and scanning microscopy in an analysis of the interaction between these strains and abiotic surfaces and cell cultures of pulmonary epithelium HL. It was shown that mutant strains with a low ability to form biofilms were characterized by a disturbed adhesion process.

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