Project description:To investigate the role of outer membrane vesicles (OMVs) and related proteins in iron acquisition mechanism of hypervirulent Klebsiella pneumoniae (HVKP) and classic Klebsiella pneumoniae (cKP).
Project description:Hypervirulent Klebsiella pneumoniae (hvKp) causes invasive infections and severe systemic inflammation. In this study, outer membrane vesicles (OMVs) derived from clinically isolated hvKp and classical K. pneumoniae (cKp) strains were characterized using an integrated proteogenomic workflow combining whole-genome sequencing and label-free LC–MS/MS proteomics. The dataset includes quantitative proteomic profiles of OMVs and whole-cell lysates together with strain-specific protein annotations for comparative analyses of OMVs cargo composition, functional annotation, and pathogenicity.
2026-07-22 | PXD045083 | Pride
Project description:multidrug-resistant Klebsiella pneumoniae from liver abscess
Project description:Klebsiella pneumoniae liver abscess (KPLA) is a severe bacterial infection complicated by intrahepatic thrombophlebitis and extrahepatic metastatic infections, leading to high mortality rates. This study investigates the role of neutrophil extracellular traps (NETs) in endothelial injury and disease progression in KPLA. Our findings demonstrate that C3 deposition on NETs significantly contributes to endothelial damage. In a KPLA mouse model, increased C3 levels were observed in the liver, with NETs carrying substantial amounts of C3, disrupting the endothelial barrier and exacerbating liver injury. Treatment with the C3 inhibitor AMY-101 reduced C3 deposition on NETs, alleviated endothelial damage, significantly improved survival, and reduced extrahepatic dissemination, inflammatory infiltration, and lung injury while also suppressing systemic inflammation. Molecular analysis revealed that the TLR4-PI3Kα-AKT signaling pathway is crucial in K. pneumoniae-induced NET formation. Our findings underscore the pivotal role of C3 in NET-mediated endothelial damage and the pathogenesis of KPLA. Thus, targeting C3 deposition on NETs may be a promising therapeutic strategy to reduce endothelial injury, thrombosis, and extrahepatic infections in KPLA without compromising neutrophil antimicrobial function.
2025-03-21 | GSE288691 | GEO
Project description:Molecular Epidemiology, Virulence, and Resistance in Hypervirulent Klebsiella pneumoniae from Liver Abscess Patients in Zhejiang, China
| PRJNA1413581 | ENA
Project description:WGS of klebsiella pneumoniae from liver abscess (LA)
