Project description:Pseudomonas aeruginosa is a virulent opportunistic pathogen responsible for high morbity in COPD, burns , implanted medical devices and cystic fibrosis. Pseudomonas aeruginosa is a problematic colonizer of the human lung. P. aeruginosa produces a phospholipase C (PlcH) that degrades choline-containing lipids such as phosphatidylcholine and sphingomylein that are found in lung surfactant and in host membranes. In this study, we analyzed gene expression in mutants defective in PlcH production (delta-plcH and delta-gbdR) and the wild type when growing in medium with lung surfactant.
Project description:Pseudomonas aeruginosa is a virulent opportunistic pathogen responsible for high morbity in COPD, burns , implanted medical devices and cystic fibrosis. Pseudomonas aeruginosa is a problematic colonizer of the human lung. P. aeruginosa produces a phospholipase C (PlcH) that degrades choline-containing lipids such as phosphatidylcholine and sphingomylein that are found in lung surfactant and in host membranes. In this study, we analyzed gene expression in mutants defective in PlcH production (delta-plcH and delta-gbdR) and the wild type when growing in medium with lung surfactant. Pseudomonas aeruginosa was cultured in liquid cultures with aeration in a defined medium with Survanta, a lung surfactant replacement. Cultures were harvested during mid-exponential phase, and RNA was isolated for microarray analysis. The P. aeruginosa strain PAO1 wild type gene expression was compared to expression profiles from delta-gbdR and delta-plcHR deletion mutants, two mutants defective in PlcH production.
Project description:Analysis of Pseudomonas aeruginosa PAO1 treated with 200 µM sphingomyelin. Results provide insight into the response to sphingomyelin in P. aeruginosa.
Project description:In the present study, we employed Affymetrix Pseudomonas aeruginosa GeneChip arrays to investigate global gene expression profiles during the cellular response of Pseudomonas aeruginosa to sodium hypochlorite Keywords: Antimicrobial response
Project description:To characterize the dynamic changes and differences of lung transcriptomic profiles induced by intratracheal infection of Neiserria subclava and Pseudomonas aeruginosa over a 14-day course.
Project description:In the present study, we employed Affymetrix Pseudomonas aeruginosa GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Pseudomonas aeruginosa to Chlorhexidine diacetate, which involved initial growth inhibition and metabolism. Keywords: Transcriptome study
Project description:In the present study, we employed Affymetrix Pseudomonas aeruginosa GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Pseudomonas aeruginosa to ortho-phenylphenol, which involved initial growth inhibition and metabolism. Keywords: Time course
Project description:Lung surfactant-derived fatty acids are a primary carbon source for the opportunistic human pathogen, Pseudomonas aeruginosa (PA), in the airways of people with cystic fibrosis. However, the mechanisms underlying the breakdown of these fatty acids by PA, as well as the potential implications of fatty acid degradation on the virulence, remain incompletely elucidated. Here, we compared the proteomes of a Manchester epidemic strain Pa10348 growing on octanoate (C8:0), palmitate (C16:0) and oleate (C18:1) with the proteome of that growing on commonly explored carbon source, glucose.
Project description:The response of bacteria to the conditions at the site of infection is a key part of the transcriptional program that will determine the sucess of the infectious agent. To model the environment of the distal airway, we used bovine pulmonary surfactant (Survanta). P. aeruginosa transcript levels were measured in the presence or absence of Survanta in MOPS minimal medium to identify transcripts altered in response to surfactant. The most highly induced transcript in Survanta was PA5325, renamed sphA based on our findings that the gene was specifically induced by sphingosine derived from the sphingomyelin present in pulmonary surfactant. A divergently transcribed transcription factor, PA5324, was demonstrated to be critical for the sphingosine dependent induction of sphA and was therefore renamed SphR. Microarrays of the sphR mutant cells were compared to wild type to determine the likely SphR regulon. Wild type and sphR mutant cells were pre-grown in MOPS minimal media and then split and resuspended in MOPS pyruvate or MOPS pyruvate + surfactant
Project description:The response of bacteria to the conditions at the site of infection is a key part of the transcriptional program that will determine the sucess of the infectious agent. To model the environment of the distal airway, we used bovine pulmonary surfactant (Survanta). P. aeruginosa transcript levels were measured in the presence or absence of Survanta in MOPS minimal medium to identify transcripts altered in response to surfactant. The most highly induced transcript in Survanta was PA5325, renamed sphA based on our findings that the gene was specifically induced by sphingosine derived from the sphingomyelin present in pulmonary surfactant. A divergently transcribed transcription factor, PA5324, was demonstrated to be critical for the sphingosine dependent induction of sphA and was therefore renamed SphR. Microarrays of the sphR mutant cells were compared to wild type to determine the likely SphR regulon.
