title: Ex vivo transcriptional profiling reveals a common set of genes important for the adaptation of Pseudomonas aeruginosa to chronically infected host sites.
abstract: The opportunistic bacterium Pseudomonas aeruginosa is a major nosocomial pathogen causing both devastating acute and chronic persistent infections. During the course of an infection, P.  aeruginosa rapidly adapts to the specific conditions within the host. In the present study, we aimed at the identification of genes that are highly expressed during biofilm infections such as in chronically infected lungs of patients with cystic fibrosis (CF), burn wounds and subcutaneous mouse tumours. We found a common subset of differentially regulated genes in all three in vivo habitats and evaluated whether their inactivation impacts on the bacterial capability to form biofilms in vitro and to establish biofilm-associated infections in a murine model. Additive effects on biofilm formation and host colonization were discovered by the combined inactivation of several highly expressed genes. However, even combined inactivation was not sufficient to abolish the establishment of an infection completely. These findings can be interpreted as evidence that either redundant traits encode functions that are essential for in vivo survival and chronic biofilm infections and/or bacterial adaptation is considerably achieved independently of transcription levels. Supplemental screens, will have to be applied in order to identify the minimal set of key genes essential for the establishment of chronic infectious diseases.
authors.affiliation: Institute for Molecular Bacteriology, Twincore, Center for Clinical and Experimental Infection Research, a joint venture of the Helmholtz Center of Infection Research and the Hannover Medical School, Hannover, 30625, Germany.
authors.forename: Piotr
authors.initials: P
authors.lastname: Bielecki
authors.forename: Uliana
authors.initials: U
authors.lastname: Komor
authors.forename: Agata
authors.initials: A
authors.lastname: Bielecka
authors.forename: Mathias
authors.initials: M
authors.lastname: Müsken
authors.forename: Jacek
authors.initials: J
authors.lastname: Puchałka
authors.forename: Mathias W
authors.initials: MW
authors.lastname: Pletz
authors.forename: Manfred
authors.initials: M
authors.lastname: Ballmann
authors.forename: Vítor A P
authors.initials: VA
authors.lastname: Martins dos Santos
authors.forename: Siegfried
authors.initials: S
authors.lastname: Weiss
authors.forename: Susanne
authors.initials: S
authors.lastname: Häussler
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics*; D000818:Animals; D018441:Biofilms; D003550:Cystic Fibrosis / Q000150:complications* / Q000382:microbiology*; D017753:Ecosystem; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D020868:Gene Silencing; D005809:Genes, Regulator; D006801:Humans; D008168:Lung / Q000382:microbiology; D051379:Mice; D009369:Neoplasms / Q000150:complications / Q000382:microbiology; D011552:Pseudomonas Infections / Q000150:complications* / Q000382:microbiology*; D011550:Pseudomonas aeruginosa / Q000235:genetics / Q000502:physiology*