Klebsiella pneumoniae is an opportunistic pathogen and it can cause human mucosal lesions through the intestine, leading to bacteremia and abscess formation in liver and spleen. Previous studies have shown that K. pneumoniae can enter or cross cells through the intestinal epithelium, but the mechanism is unknown. In this study, we treated the intestinal epithelial cell line Caco-2 with KP1195, a clinically isolated strain with high adhesion and invasion of intestinal epithelial cells. The results showed that the treatment of K. pneumoniae could increase the expression of integrin gene and further disrupt the changes of cytoskeleton. Treating Caco-2 with cytoskeletal inhibitor cytorelaxin D can significantly increase the efficiency of K. pneumoniae invading Caco-2 cells. These data suggest that disruption of the cytoskeleton through integrins may be one of the mechanisms by which K. pneumoniae increases intracellular invasion. This study provides a theoretical basis for further understanding of the mechanism of K. pneumoniae entering intestinal epithelial cells.
Keyphrases
- klebsiella pneumoniae
- cell migration
- escherichia coli
- multidrug resistant
- induced apoptosis
- cell cycle arrest
- respiratory tract
- endothelial cells
- poor prognosis
- staphylococcus aureus
- cell death
- cell proliferation
- copy number
- pseudomonas aeruginosa
- dna methylation
- reactive oxygen species
- cystic fibrosis
- deep learning
- data analysis