A gacS deletion in Pseudomonas aeruginosa cystic fibrosis isolate CHA shapes its virulence

• Published in: PloS one Vol. 9; no. 4; p. e95936
• Main Authors: Sall, Khady Mayebine, Casabona, Maria Guillermina, Bordi, Christophe, Huber, Philippe, de Bentzmann, Sophie, Attrée, Ina, Elsen, Sylvie
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.04.2014; Public Library of Science (PLoS)
• Subjects: Alginic acid; Amino Acid Sequence; Antibiotics; Bacterial Proteins - chemistry; Bacterial Proteins - genetics; Bacteriology; Biofilms; Biology; Biology and Life Sciences; Cancer; Care and treatment; Chronic illnesses; Cystic fibrosis; Cystic Fibrosis - microbiology; Diagnosis; Evolution & development; Flagella; Gene Deletion; Gene expression; Genes, Bacterial; Health aspects; Infections; Kinases; Life Sciences; Lungs; Machinery; Machinery and equipment; Medicine and Health Sciences; Microbiology and Parasitology; Molecular Sequence Data; Mutation; Opportunist infection; Pathogenesis; Phagocytosis; Phase transitions; Pili; Polymerase Chain Reaction; Polysaccharides; Pseudomonas; Pseudomonas aeruginosa; Pseudomonas aeruginosa - genetics; Pseudomonas aeruginosa - isolation & purification; Pseudomonas aeruginosa - pathogenicity; Risk factors; Saccharides; Secretion; Sequence Homology, Amino Acid; Silence; Virulence; Virulence - genetics; Virulence factors; France; Polymerase chain reaction; Pathogen motility; Virulence factors; Plasmid construction; Cystic fibrosis; Pseudomonas aeruginosa; Gene expression; DNA transcription
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0095936

Pseudomonas aeruginosa, a human opportunistic pathogen, is capable of provoking acute and chronic infections that are associated with defined sets of virulence factors. During chronic infections, the bacterium accumulates mutations that silence some and activate other genes. Here we show that the cystic fibrosis isolate CHA exhibits a unique virulence phenotype featuring a mucoid morphology, an active Type III Secretion System (T3SS, hallmark of acute infections), and no Type VI Secretion System (H1-T6SS). This virulence profile is due to a 426 bp deletion in the 3' end of the gacS gene encoding an essential regulatory protein. The absence of GacS disturbs the Gac/Rsm pathway leading to depletion of the small regulatory RNAs RsmY/RsmZ and, in consequence, to expression of T3SS, while switching off the expression of H1-T6SS and Pel polysaccharides. The CHA isolate also exhibits full ability to swim and twitch, due to active flagellum and Type IVa pili. Thus, unlike the classical scheme of balance between virulence factors, clinical strains may adapt to a local niche by expressing both alginate exopolysaccharide, a hallmark of membrane stress that protects from antibiotic action, host defences and phagocytosis, and efficient T3S machinery that is considered as an aggressive virulence factor.