| Description |
Bacterial pneumonia still affects human health. Klebsiella pneumoniae, an opportunistic pathogen, is among the common bacterial pneumonia-causing pathogens. However, how to rapidly detect K. pneumoniae in infected tissues remains unclear. The mechanism underlying K. pneumoniae infection remains incompletely elucidated, especially during early infection. In vivo experiments revealed that during infection, K. pneumoniae enters airway epithelial cells, damages the vascular endothelial barrier, recruits macrophages to the infection site, and polarizes macrophages to the M1 type. To clarify how K. pneumoniae exerts this series of effects through airway epithelial cells, single-cell Raman spectroscopy was performed. K. pneumoniae was rapidly detected in the infected cells and tissues, and the expression of lipid substances was significantly increased in the infected cells. To further clarify how lipid substances functioned in the infected cells, we conducted metabolomics analysis of exosomes from K. pneumoniae-infected epithelial cells. Phosphatidylcholine expression in the exosomes significantly increased. Consequently, the tight junction between the vascular endothelial cells was destroyed, and macrophages were infiltrated and polarized to M1 macrophages. The NF-κB signaling pathway in the cells was activated, inflammatory factor and chemokine expression was increased, and neutrophils were recruited. These results were further validated in K. pneumoniae-infected tissues. |
