Expression of the lipopolysaccharide biosynthesis gene lpxD affects biofilm formation of Pseudomonas aeruginosa
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ORIGINAL PAPER
Expression of the lipopolysaccharide biosynthesis gene lpxD affects biofilm formation of Pseudomonas aeruginosa Sahar A. Alshalchi · Gregory G. Anderson
Received: 9 July 2014 / Revised: 13 August 2014 / Accepted: 15 August 2014 / Published online: 31 August 2014 © Springer-Verlag Berlin Heidelberg 2014
Abstract Bacterial biofilms are an important cause of nosocomial infections. Microorganisms such as Pseu‑ domonas aeruginosa colonize biotic and abiotic surfaces leading to chronic infections that are difficult to eradicate. To characterize novel genes involved in biofilm formation, we identified the lpxD gene from a transposon-mutant library of P. aeruginosa. This gene encodes a glucosamineN acyltransferase, which is important for lipopolysaccharide biosynthesis. Our results showed that a loss-of-expression mutant of lpxD was defective for biofilm formation on biotic and abiotic surfaces. Additionally, this mutant strain exhibited significantly decreased bacterial attachment to cultured airway epithelial cells, as well as increased bacterial cytotoxicity toward airway cells. However, consistent with a defect in lipid A structure, airway cells incubated with the lpxD mutant or with mutant lipid A extracts exhibited decreased IL-8 production and necrosis, respectively. Overall, our data indicate that manipulating lpxD expression may influence P. aeruginosa’s ability to establish biofilm infections. Keywords Lipopolysaccharide · Biofilm · Pseudomonas aeruginosa · Cystic fibrosis · Necrosis
Communicated by Erko Stackebrandt. S. A. Alshalchi · G. G. Anderson (*) Department of Biology, Indiana University Purdue University Indianapolis, 723 West Michigan Street, SL 320, Indianapolis, IN 46202, USA e-mail: [email protected]
Introduction Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen, commonly isolated from infections associated with biofilm formation, including infections of burns and other wounds, otitis media, and complicated lung infections of patients with cystic fibrosis (CF). In fact, it is regarded as one of the most medically relevant biofilm forming bacterial species, contributing significantly to morbidity and mortality in CF patients (Costerton et al. 1999; Gibson et al. 2003; Doring et al. 2011). P. aeruginosa biofilm cells are embedded in a complex matrix of polysaccharides, proteins, and extracellular DNA (eDNA), which protect the bacteria from phagocytes, deleterious compounds released from immune cells, and antimicrobial treatment (Davey and O’Toole 2000; Ryder et al. 2007; Doring et al. 2011). Eventually, persistence of P. aeruginosa in CF patients and the resultant chronic inflammation lead to airway destruction and fibrosis. Bacterial colonization becomes lifelong, contributing to CF patient complications, including respiratory failure and death (Costerton et al. 1999; Doring et al. 2011). The expression of virulence genes in P. aeruginosa has been shown to be reciprocally regulated, with some factors produced during chronic infections, associated with biofilm formation
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