Purpose. Pseudomonas aeruginosa is one of the agents that are commonly implicated in nosocomial infections. However, it is also present as a commensal in various body sites of healthy persons, making the diagnosis of infection by culture difficult. A number of virulence factors expressed by the organism have been implicated in its pathogenicity. We undertook this study to identify the host and organism factors associated with infection.
Methodology. Pathogenic, colonizing and environmental isolates were tested for apr, lasB, the T3SS effector exoenzymes (exoS, exoT, exoU and exoY) and toxA genes, biofilm production and antimicrobial susceptibility. The isolates were further typed by RAPD.
Results. Eighty-seven isolates from 61 patients, including 11 environmental isolates, were obtained. None of the virulence factors were found to be significantly associated with infection, and nor was the antimicrobial susceptibility. The presence of the exoU gene and infection by MDR strains correlated significantly with the duration of hospital stay. Positivity for exoS and exoU genes was found to be strongly correlated with multi-drug resistance. exoU positivity correlated strongly with fluoroquinolone resistance. Sinks in the ward and intensive care unit were found to be a niche for XDR P. aeruginosa. Eighty-five isolates were typeable using the ERIC2 primer, showing 71 distinct RAPD patterns with >15 % difference in UPGMA-generated dice coefficients.
Conclusions. exoU positivity is associated with severe disease, as evidenced by the longer duration of hospital stay of these patients. However, the presence of virulence factors or multi-drug resistance in the cultured strain should not prompt the administration of anti-pseudomonal chemotherapy.
Purpose. Nodal may play an important role in the development of cancers. The present study was designed to determine the effects of Nodal induced by respiratory syncytial virus (RSV) infection on the occurrence and development of lung cancer and the underlying mechanisms.
Methodology. After verification of RSV infection by observation of cytopathic effect and indirect immunofluorescence, real-time PCR, Western blot and methylation assays were used to verify the influence of RSV on Nodal expression. Then, a Nodal overexpressed vector was constructed and the effects of Nodal on the proliferation and apoptosis of bronchial epithelial cells (BECs) and epithelial-mesenchymal transition (EMT) were assayed by flow cytometry and Western blot, respectively. Moreover, Lefty and pSmad2/3 were assayed by Western blot and Cyclin D1, CDK4, c-myc and Bcl-2 induced by Nodal overepression or RSV infection were also assayed by real-time PCR.
Results. The results showed that Nodal over expression and demethylation of the promoter were observed in BECs after RSV infection. Activation of Nodal promoted proliferation, colony formation and EMT and inhibited apoptosis of BECs. Nodal also promoted malignant change by promoting expression of cyclin D1 and related-dependent kinase and inhibiting apoptosis. Besides, RSV infection inhibited Lefty expression and promoted the activation of pSmad2/3. RSV also promoted Cyclin D1, CDK4, c-myc and Bcl-2 expression through the activation of pSmad2/3.
Conclusions. Our data showed that persistence of RSV promoted the proliferation, epithelial-mesenchymal transition and expression of oncogenes through Nodal signaling, which may be associated with the occurrence and development of lung cancers.