Min K.B.,Brain Korea PLUS Project for Medical Science |
Lee K..-M.,Brain Korea PLUS Project for Medical Science |
Oh Y.T.,Brain Korea PLUS Project for Medical Science |
Yoon S.S.,Brain Korea PLUS Project for Medical Science |
Yoon S.S.,Yonsei University
FEMS Microbiology Letters | Year: 2014
Alginate-overproducing mucoid Pseudomonas aeruginosa, responsible for chronic airway infections in cystic fibrosis (CF) patients, is resistant to antibiotic treatments and host immune clearance. In this study, we performed a phenotype microarray screen and identified sulfate ion as a molecule that can suppress alginate production. When a mucoid P. aeruginosa strain CM21 and additional mucoid isolates were grown with 5% sodium sulfate, significantly decreased levels of alginate were produced. Suppression of alginate production was also induced by other sulfate salts. Expression of a reporter gene fused to the algD promoter was considerably decreased when grown with sulfate. Furthermore, bacterial cell shape was abnormally altered in CM21, but not in PAO1, a prototype nonmucoid strain, suggesting that sulfate-stimulated cell shape change is associated with transcriptional suppression of the alginate operon. Finally, a CM21 lpxC mutant defective in lipid A biosynthesis continued to produce alginate and maintained the correct cell shape when grown with sulfate. These results suggest a potential involvement of lipoploysaccharide biosynthesis in the sulfate-induced reversion to nonmucoid phenotype. This study proposes a novel strategy that can be potentially applied to treat persistent infection by recalcitrant mucoid P. aeruginosa. Alginate-overproducing mucoid Pseudomonas aeruginosa are resistant to many stress conditions; here we show that alginate production is suppressed by sulfate, suggesting that sulfate compounds could be used to down-regulate the virulence of mucoid P. aeruginosa. © 2014 Federation of European Microbiological Societies. Published by John Wiley & Sons Ltd. All rights reserved.