Project description:Carbapenem-resistant Klebsiella pneumoniae (CRKP), particularly the K64 serotype, poses a severe clinical threat due to its high virulence and multidrug resistance. In this study, we investigated the gene expression profiles of host lung tissues to understand the pathogenesis of K64-CRKP infection and the therapeutic mechanism of Dep44, a capsule-degrading depolymerase. An acute pneumonia mouse model was established via intranasal infection with K64-CRKP. We performed high-throughput RNA sequencing (RNA-seq) on lung tissues from four experimental groups: the negative control group (healthy mice), the positive control group (K64-CRKP infected model), the treatment group (infected mice treated with Dep44), and the drug control group (healthy mice treated with Dep44). The analysis aims to elucidate the host immune response to K64-CRKP infection and evaluate how Dep44 treatment modulates these transcriptomic changes to exert its therapeutic effect.
Project description:Detailed exploration was performed on the T cell and B cell transcriptional profiles when comparing moderate and severe patients to healthy donors, identifying candidate gene signatures. Furthermore, we analyzed the properties of cytotoxicity and exhaustion within T cell subgroups derived from CRKP samples.
Project description:Meropenem is one of the main antibiotics used in the clinical treatment of CRKP. This study demonstrated that some important metabolic changes occurred in Meropenem-induced CRKP-OMVs, The OMVs proteome expression profile indicates increased secretion of stress proteins released from Meropenem-induced Klebsiella pneumoniae. Furthermore, this is the first study to discuss the protein-protein interaction network of the OMVs released by CRKP, especially under antibiotic stress.
