1Suzhou Medical College of Soochow University, Suzhou, People's Republic of China.
2Department of Laboratory Medicine, Affiliated Wuxi Fifth Hospital of Jiangnan University, Wuxi 214005, China.
Acta Microbiol Immunol Hung. 2024 Jul 30;71(3):237-241. doi: 10.1556/030.2024.02326. Print 2024 Sep 18.
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.
肺炎克雷伯菌是一种机会致病菌，它可以通过肠道引起人类黏膜损伤，导致菌血症和肝脾脓肿形成。先前的研究表明，肺炎克雷伯菌可以通过肠上皮细胞进入或穿过细胞，但具体机制尚不清楚。在这项研究中，我们用 KP1195 处理肠上皮细胞系 Caco-2，KP1195 是一种具有高黏附性和侵袭性的临床分离株，能侵袭肠上皮细胞。结果表明，肺炎克雷伯菌处理可以增加整合素基因的表达，进一步破坏细胞骨架的变化。用细胞骨架抑制剂细胞松弛素 D 处理 Caco-2 可以显著提高肺炎克雷伯菌侵袭 Caco-2 细胞的效率。这些数据表明，通过整合素破坏细胞骨架可能是肺炎克雷伯菌增加细胞内侵袭的机制之一。本研究为进一步了解肺炎克雷伯菌进入肠上皮细胞的机制提供了理论依据。
