Project description:Staphylococcus aureus is an opportunistic pathogen capable of causing various infections ranging from superficial skin infections to life-threatening severe diseases, including pneumonia and sepsis. This bacterium is attached to biotic and abiotic surfaces and forms biofilms that are resistant to conventional antimicrobial agents and clearance by host defenses. Infections associated with biofilms may result in longer hospitalizations, a need for surgery, and may even result in death. Agents that inhibit the formation of biofilms and virulence without affecting bacterial growth to avoid the development of drug resistance could be useful for therapeutic purposes. In this regard, we identified and isolated a small cyclic peptide, gurmarin, from a plant source that inhibited the formation of S. aureus biofilm without affecting the growth rate of the bacterium. We determined the gene expression of S. aureus biofilm treated with gurmarin and compared it to the untreated control biofilms. Differentially expressed genes were identified and their roles in the inhibition of S. aureus biofilms by gurmarin were analyzed.
Project description:Legionella pneumophila (Lp) is a waterborne bacterium able to infect human alveolar macrophages, causing a severe pneumonia known as Legionnaires’ disease. In water, Lp grows inside ciliates and ameoba. Lp is able to survive for several months in water, while searching for host cells. In Lp, the sigma factor RpoS is important for survival in water. Several small regulatory RNAs (sRNA) are known to regulate the expression of RpoS in other bacteria. A previous transcriptomic study showed that RpoS positively regulates the sRNA Lpr10 in Lp. Microarray analysis was performed to investigate the genes regulated by Lpr10.
2020-05-27 | GSE151162 | GEO
Project description:Meta-transcriptomes of patients with pneumonia and acute respiratory infections
Project description:Human bocavirus (HBoV) is a newly discovered parvovirus identified from pooled nasopharyngeal aspirate specimens. Human bocavirus 1 (HBoV1) is a respiratory virus observed in respiratory samples from small children presenting bronchiolitis, wheezing, cough, fever, and rhinorrhea. It is the fourth most common virus detected in respiratory infections. DNA of HBoV1 was detected in up to 18% of nasal or nasopharyngeal samples and another study has been shown that over than 85% of children in the United States have antibodies to this virus. HBoV1 is a small DNA virus with a nonenveloped icosahedral capsid. This virus previously has been associated with wheezing, acute otitis media, severe pneumonia and respiratory failure. HBoV 1 has been also detected in the blood of acute respiratory patients and the selected group of immunocompromised children and also determined in healthy blood donors. The role of HBoV1 in the inflammatory process is poorly known. The aim of this project is to clarify the role of HBOV1 in the immunoregulatory mechanisms.
Project description:The onset of an infection-specific transcriptional program precedes the clinical diagnosis in patients who developed Ventilator-associated pneumonia (VAP). Ventilator-associated tracheobronchitis (VAT) is another respiratory infection affecting<br><br>outcomes in intubated patients, but interactions between VAT and VAP remains unknown.
Project description:This project was a prospective translational study aimed at evaluating gene expression profiles (GEP) of patients with ventilator-associated pneumonia (VAP) . GEP of VAP were compared with a control group of patients which did not developed ventilator-associated lower respiratory tract infection despite being subjected to mechanical ventilation.
Project description:Streptococcus pneumoniae normally resides in the human nasopharynx in a non-disease state. In response to yet unknown triggers it can descend to the lower respiratory tract and/or invade the bloodstream. Regulation and activation of virulence genes play essential roles in this process of disease development. A putative transcriptional regulator in S. pneumoniae, MgrA, with homology to a virulence gene activator, mga, of Group A streptococcus (GAS) was previously identified as being required for development of pneumonia in a murine model. In this work we confirm that mgrA is required for both nasopharyngeal carriage and pneumonia. Transcriptional profiling by microarray technology through the growth course of a strain that bears a deletion of mgrA (AC1500) with that of a strain that over expresses Mgra (AC1481) is used to show that MgrA acts as a repressor of the previously characterized rlrA pathogenicity islet. This is manifested phenotypically by a decrease in adherence to epithelial cells in tissue culture since rlrA pathogenicity islet contains genes mediating adherence.
