Data set related to the article: "Klebsiella pneumoniae-OMVs activate death-signaling pathways in Human Bronchial Epithelial Host Cells (BEAS-2B)"

The programmed cell death pathways of apoptosis are important in mammalian cellular protectionfrom infections. The activation of these pathways depends on the presence of membranereceptors that bind bacterial components to activate the transduction mechanism. In addition tobacteria, these mechanisms can be activated by outer membrane vesicles (OMVs). OMVs arespherical vesicles of 20–250 nm diameter, constitutively released by Gram-negative bacteria.They contain several bacterial determinants including proteins, DNA/RNA and proteins, thatactivate different cellular processes in host cells. This study focused on Klebsiella pneumoniae-OMVs in activating death mechanisms in human bronchial epithelial cells (BEAS-2B). Characterizationof purified OMVs was achieved by scanning electron microscopy, nanoparticle trackinganalysis and protein profiling. Cell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay while apoptotic induction was measured by flow cytometryand confirmed by western blotting. The OMVs produced showed a spherical morphology, with adiameter of 137.2 ± 41 nm and a vesicular density of 7.8 × 109 particles/mL Exposure of cellmonolayers to 50 μg of K. pneumoniae-OMV for 14 h resulted in approximately 25 % cytotoxicityand 41.15–41.14 % of cells undergoing early and late apoptosis. Fluorescence microscopyrevealed reduced cellular density, the presence of apoptotic bodies, chromatin condensation, andnuclear membrane blebbing in residual cells. Activation of caspases 􀀀 3 and 􀀀 9 and dysregulationof BAX, BIM and Bcl-xL indicated the activation of mitochondria-dependent apoptosis. Furthermore,a decrease in the antioxidant enzymes superoxide dismutase, catalase and glutathioneperoxidase involved endoplasmic reticulum stress with the potential formation of reactive oxygen species.

These findings provide evidence for the role of OMVs in apoptosis and involvement in thepathogenesis of K. pneumoniae infections.