Pseudomonas aeruginosa Type IV pilus and resistance to the antimicrobial properties of surfactant protein-A
type: CreativeWork
description: The lung contains numerous innate immune cells and effector proteins. One important component of this immune system is the surfactant protein-A (SP-A), which facilitates microbial clearance by opsonization and membrane permeabilization. Pseudomonas aeruginosa (PA) is a major Gram-negative bacterial pathogen commonly associated with chronic lung infection in cystic fibrosis. In order to resist the antibacterial effects of SP-A, PA expresses various structural and secreted virulence factors. Previously, Wu et al (2003) have shown that Escherichia coli lipopolysaccharides (LPS) are important in resisting SP-A-mediated membrane permeabilization. Zhang et al (2005) performed a comparative signature-tagged mutagenesis screen to identify PA virulence factors needed to resist SP-A-mediated lung clearance, and identified PchA (isochorismate synthase) and PtsP (phosphoenolpyruvate protein phosphotransferase) as important for resisting SP-A-mediated membrane permeability. Zhang et al (2007) further showed that PA flagellum is important for resisting SP-A-mediated membrane permeabilization. Finally, Kuang et al (2011) have shown PA elastase degrades SP-A, allowing an avenue for PA to escape SP-A-mediated opsonization and membrane permeabilization. In this study, we demonstrated that type IV pilus (Tfp) is important in the resistance of lung clearance both in the presence and absence of SP-A. The Tfp-deficient mutant, ΔpilA, is severely attenuated in an acute pneumonia model of infection in the lungs of wild-type mice that it allows similar bacterial load as PAO1 in the lungs of SP-A-/- mice. The ΔpilA bacteria are more susceptible to SP-A-mediated aggregation and opsonization. In addition, the integrity of the outer membranes of ΔpilA bacteria is compromised, rendering them more susceptible to SP-A-mediated membrane permeabilization. By using Tfp extension and retraction mutants, we demonstrate that the increased susceptibility of ΔpilA to SP-A-mediated opsonization is caused b…
abstract: The lung contains numerous innate immune cells and effector proteins. One important component of this immune system is the surfactant protein-A (SP-A), which facilitates microbial clearance by opsonization and membrane permeabilization. Pseudomonas aeruginosa (PA) is a major Gram-negative bacterial pathogen commonly associated with chronic lung infection in cystic fibrosis. In order to resist the antibacterial effects of SP-A, PA expresses various structural and secreted virulence factors. Previously, Wu et al (2003) have shown that Escherichia coli lipopolysaccharides (LPS) are important in resisting SP-A-mediated membrane permeabilization. Zhang et al (2005) performed a comparative signature-tagged mutagenesis screen to identify PA virulence factors needed to resist SP-A-mediated lung clearance, and identified PchA (isochorismate synthase) and PtsP (phosphoenolpyruvate protein phosphotransferase) as important for resisting SP-A-mediated membrane permeability. Zhang et al (2007) further showed that PA flagellum is important for resisting SP-A-mediated membrane permeabilization. Finally, Kuang et al (2011) have shown PA elastase degrades SP-A, allowing an avenue for PA to escape SP-A-mediated opsonization and membrane permeabilization. In this study, we demonstrated that type IV pilus (Tfp) is important in the resistance of lung clearance both in the presence and absence of SP-A. The Tfp-deficient mutant, ΔpilA, is severely attenuated in an acute pneumonia model of infection in the lungs of wild-type mice that it allows similar bacterial load as PAO1 in the lungs of SP-A-/- mice. The ΔpilA bacteria are more susceptible to SP-A-mediated aggregation and opsonization. In addition, the integrity of the outer membranes of ΔpilA bacteria is compromised, rendering them more susceptible to SP-A-mediated membrane permeabilization. By using Tfp extension and retraction mutants, we demonstrate that the increased susceptibility of ΔpilA to SP-A-mediated opsonization is caused b…
author: Tan, Rommel Max
language: en
keywords: Pseudomonas aeruginosa, Surfactant protein-A, Type IV pilus
date published: 2014-01-16T18:25:08Z
date modified: 2026-07-22T22:25:38Z
provider: University of Illinois - Urbana-Champaign
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Illinois at Urbana-Champaign

PropertyValue
property ID: Handle
value: http://hdl.handle.net/2142/46882