Session 1E: Role of Pyocyanin, a Secreted Virulence Factor of Pseudomonas aeurignosa, in Respiratory Epithelial Cell Functions
Session Number
Session 1E: 1st Presentation
Advisor(s)
Viswanathan Natarajan, University of Illinois at Chicago
Location
Room A113
Start Date
28-4-2017 8:30 AM
End Date
28-4-2017 9:45 AM
Abstract
Pseudomonas aeruginosa (PA) is a rod-shaped gram negative bacterium that is associated with lung infection of humans with compromised host-defense such as cystic fibrosis. PA secretes proteins, lipopolysaccharides and virulence factors such as pyocyanin (PCN) that modulate host cell signal transduction and immune responses. PCN mediates its cellular effects via reactive oxygen species (ROS) production in host cells. However, molecular mechanism(s) of PCN-induced ROS production are not well understood. In this study, we will address PCN mediated regulation of ROS via MAPK signaling and activation of NADPH Oxidase (NOX) proteins in bronchial epithelium. Specifically, the role of PCN on ROS generated by mitochondria, NOX2 and NOX4 and endoplasmic stress will be determined using cellular and molecular approaches. In addition, the role of PCN-induced ROS on epithelial barrier integrity and secretion of pro-inflammatory cytokines will be investigated using bronchial epithelial cells in culture. These planned studies will provide new and novel information on PCN-mediated cellular responses in host immune responses in the bronchial epithelium.
Session 1E: Role of Pyocyanin, a Secreted Virulence Factor of Pseudomonas aeurignosa, in Respiratory Epithelial Cell Functions
Room A113
Pseudomonas aeruginosa (PA) is a rod-shaped gram negative bacterium that is associated with lung infection of humans with compromised host-defense such as cystic fibrosis. PA secretes proteins, lipopolysaccharides and virulence factors such as pyocyanin (PCN) that modulate host cell signal transduction and immune responses. PCN mediates its cellular effects via reactive oxygen species (ROS) production in host cells. However, molecular mechanism(s) of PCN-induced ROS production are not well understood. In this study, we will address PCN mediated regulation of ROS via MAPK signaling and activation of NADPH Oxidase (NOX) proteins in bronchial epithelium. Specifically, the role of PCN on ROS generated by mitochondria, NOX2 and NOX4 and endoplasmic stress will be determined using cellular and molecular approaches. In addition, the role of PCN-induced ROS on epithelial barrier integrity and secretion of pro-inflammatory cytokines will be investigated using bronchial epithelial cells in culture. These planned studies will provide new and novel information on PCN-mediated cellular responses in host immune responses in the bronchial epithelium.