Project description:ErfA is a transcription factor of Pseudomonas aeruginosa. We here define the genome-wide binding sites of ErfA by DAP-seq in Pseudomonas aeruginosa PAO1 and IHMA87, Pseudomonas chlororaphis PA23, Pseudomonas protegens CHA0 and Pseudomonas putida KT2440.
Project description:Pseudomonas aeruginosa is a common bacterium in the terminal plumbing system of buildings and it is from this niche that a substantial fraction of infections are acquired. To better understand P. aeruginosa biology in this environment, we examined the transcriptomes in tap water and pond water.
Project description:Chronic lung infections and presistent inflammation are a leading cause of morbidity and mortality in people with cystic fibrosis and therefore there is a need for therapies that can simultaneously eliminate infection and the hyperinflammatory lung environment in CF. Mesenchymal stromal cell-derived extracellular vesicles (MSC EVs) represent a promising solution, offering potent anti-inflammatory, immunomodulatory, and antimicrobial properties while being safe and non-toxic. This study demonstrates the efficacy of MSC EVs in a CF mouse model of acute Pseudomonas aeruginosa lung infection. MSC EVs reduced Pseudomonas burden, immune cell infiltration, and pro-inflammatory cytokine levels in the lungs.
Project description:We use high-throughput sequencing to profile the response of the opportunistic mucosal pathogen Pseudomonas aeruginosa to mucins and mucin-glycans from the mucosal niche. We find that P. aeruginosa undergoes a genome-wide phenotypic shift in response to mucins and their attached glycans. Specifically, nearly all virulence pathways are downregulated in response to these host-produced factors. This study provides a framework for understanding how the host environment regulates bacterial function.
Project description:We use high-throughput sequencing to profile the response of the opportunistic mucosal pathogen Pseudomonas aeruginosa to mucins and mucin-glycans from the mucosal niche. We find that P. aeruginosa undergoes a genome-wide phenotypic shift in response to mucins and their attached glycans. Specifically, nearly all virulence pathways are downregulated in response to these host-produced factors. This study provides a framework for understanding how the host environment regulates bacterial function.
