Inactivation of Type 3 Fimbriae Increases Adhesion of Klebsiella oxytoca to Lung Epithelial Cells

Klebsiella oxytoca is a causative agent of various community-acquired and nosocomial infections, including urinary tract infections, nosocomial pneumonia, antibiotic-associated diarrhea, etc. However, the virulence factors of the species are still incompletely understood. The adhesive potential of the urological isolate K. oxytoca NK-1 was characterized using several substrates. The strain was found to efficiently adhere to epithelial cell lines, glycosylated and nonglycosylated proteins, and polystyrene and to induce yeast cell agglutination, indicating the presence of type 1 and type 3 fimbriae, which are organelles that facilitate adhesion of enterobacteria to a wide range of substrates. Both type 1 and type 3 fimbrial operons were identified in the strain genome, the latter occurring in two copies. Mutants with inactivated fimbrial genes were constructed. Inactivation of type 1 fimbrial genes did not affect bacterial adhesion. Inactivation of type 3 fimbrial genes increased adhesion of K. oxytoca NK-1 to lung epithelial cells (line H1299), and mannose was shown to serve as an additional inducer of higher adhesion. Adhesion of the mutant to other substrates was not affected. The findings suggested a multifactorial nature for the K. oxytoca adhesive apparatus and the possibility of compensatory expression or overexpression of genes for alternative adhesins in the absence of type 1 and/or 3 fimbriae.