Open AccessNonmucoid conversion of mucoid Pseudomonas aeruginosa induced by sulfate‐stimulated growth
Author(s) -
Min Kyung Bae,
Lee KangMu,
Oh Young Taek,
Yoon Sang Sun
Publication year - 2014
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/1574-6968.12600
Subject(s) - pseudomonas aeruginosa , microbiology and biotechnology , sulfate , pseudomonadaceae , biology , mutant , pseudomonadales , bacteria , chemistry , biochemistry , gene , genetics , organic chemistry
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 CM 21 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 CM 21, but not in PAO 1, a prototype nonmucoid strain, suggesting that sulfate‐stimulated cell shape change is associated with transcriptional suppression of the alginate operon. Finally, a CM 21 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 .