Klebsiella pneumoniae is an opportunistic pathogenic bacterium that commonly causes pneumonia in elderly people. OmpA, a toxin that is highly expressed in the outer membrane of the bacterium, is one of the primary factors implicated in the pulmonary pathogenesis of K. pneumoniae. To evaluate the associated pyroptosis mechanism of infection, the ompA gene was cloned, and the protein was expressed, extracted, and used to treat human larynx epithelial cells. We observed that OmpA induces reactive oxygen species production and cell-cycle arrest in the G2/M phase in host cells, leading to subsequent apoptosis. Moreover, OmpA was found to induce IL-1β and IL-18 production in host cells, resulting in caspase-1 activation, which simultaneously stimulated pyroptosis, thus leading to the death of the host cells. We next sought to examine differential gene expression via RNA sequencing to better elucidate the mechanisms associated with these cellular changes, and found that genes associated with these pathways were more highly expressed in OmpA-treated cells than in K. pneumoniae-infected cells. Thus, cell-cycle arrest, apoptosis, and pyroptosis may serve as the primary defenses employed by host cells against OmpA. These results provide novel insights into the host defense against K. pneumoniae infection.

肺炎克雷伯菌是一种机会致病性细菌，通常在老年人中引起肺炎。OmpA是一种在细菌外膜中高度表达的毒素，是与肺炎克雷伯菌的肺部发病有关的主要因素之一。为了评估感染的相关凋亡机制，ompA该基因被克隆，该蛋白被表达，提取并用于治疗人喉上皮细胞。我们观察到，OmpA在宿主细胞的G2 / M期诱导活性氧的产生和细胞周期停滞，从而导致随后的细胞凋亡。此外，发现OmpA诱导宿主细胞中IL-1β和IL-18的产生，导致caspase-1激活，同时刺激发烧，从而导致宿主细胞死亡。接下来，我们试图通过RNA测序检查差异基因表达，以更好地阐明与这些细胞变化相关的机制，并发现与这些途径相关的基因在经OmpA处理的细胞中比在肺炎克雷伯菌中的表达更高。感染的细胞。因此，细胞周期停滞，凋亡和发烧可能是宿主细胞抵抗OmpA的主要防御手段。这些结果为抵抗肺炎克雷伯菌感染的宿主防御提供了新颖的见解。