Background Klebsiella pneumoniae is a prominent nosocomial pathogen that accounts for up to 10 % of all hospital-acquired infections. It is a frequent cause of ventilator-associated pneumonia (VAP). The purpose of this study was to investigate the clinical characteristics of K. pneumoniae-associated VAP and the molecular characteristics of K. pneumoniae strains.MethodsWe retrospectively reviewed 70 mechanically ventilated patients with K. pneumoniae isolated. All K. pneumoniae strains were examined to determine hypermucoviscosity (HV) phenotype, capsular serotypes, virulence genes, multilocus sequence typing and antimicrobial susceptibility.ResultsHypermucoviscosity was found in 14 of 70 (20 %) isolates of K. pneumoniae. Among the 70 patients, 43 cases (61.4 %) developed VAP. Furthermore, VAP was more frequently induced by HV-positive K. pneumoniae (14/14, 100 %) than by HV-negative strains (29/56, 51.7 %). HV-positive K. pneumoniae-associated VAP patients were more inclined to develop bacteremia and had a higher mortality rate than HV-negative strains VAP patients. Antibiotic resistance was more frequent in HV- negative strains- than in HV- positive strains-infected patients. The prevalence of rmpA and aerobactin genes were 85.7 % and 85.7 % respectively, and serotypes K1 and K2 accounted for 14.3 % and 28.6 % of the hypermucoviscosity strains, respectively. Strains carrying rmpA and aerobactin genes were significantly associated with HV-phenotype, and rmpA and aerobactin coexisted in HV-positive strains. Multilocus sequence typing analysis identified 24 different sequence types from K. pneumoniae VAP samples.ConclusionsHV-phenotype is the major virulence determinant for mechanically ventilated patients. There was a specific sequence typing (ST) distribution between HV-positive and HV-negative strains.
This study aimed at investigating the effect of microRNA‐150 (miR‐150) on cell proliferation of Burkitt lymphoma and its molecular mechanism. Gene expression analysis was applied to identify target genes of miR‐150 in Burkitt lymphoma cell line ST486 based on the dataset from the Gene Expression Omnibus (GEO) datasets GSE86432. miRNA mimics, inhibitor and small interfering RNA (siRNA) were fluorescently labeled by Cy3, whereas plasmid vector was labeled by EGFP. Cells were viewed by fluorescence microscope and transfection efficiency was evaluated through fluorescent cell percentage. Quantitative real‐time polymerase chain reaction analysis (qRT‐PCR) and western blot were applied to detect the expression level of miR‐150 and LMO4. Cell proliferation, cell cycle, and apoptosis were explored by CCK‐8, flow cytometry. Targeting relationship was validated by the Luciferase reporter assay. Tumor xenograft and immunohistochemical analysis were conducted in nude mice model. In Burkitt lymphoma cells, miR‐150 expression was significantly lower than normal ones, whereas the expression of LMO4 was upregulated. miR‐150 might inhibit cell proliferation and promoted apoptosis in Burkitt lymphoma deterioration by downregulating LMO4. The results of tumor xenograft further confirmed the role of miR‐150 in Burkitt lymphoma. Targeting LMO4 is a significant mechanism by which miR‐150 suppresses cell growth and promotes apoptosis in Burkitt lymphoma cells, thus may provide a novel target for Burkitt lymphoma therapy in the future.
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