aeruginosa mutants altered in their capacity to inhibit growth of S. aeruginosa mutants affected in growth in the presence of S. aeruginosa genes required for direct and exploitative competition.
In this perspective we developed a broad genetic screen to identify P. Increasing our understanding of these interactions is crucial ( Bragonzi et al., 2012) and might lead to the identification of new targets aiming at manipulating interactions inside polymicrobial communities to the disadvantage of pathogens such as P. This indicates that interspecies competition and cooperation play an important role in shaping composition and structure of polymicrobial bacterial populations, thereby potentially influencing disease progression. aureus, leading to an increased resistance of the latter to aminoglycoside antibiotics ( Hoffman et al., 2006). aeruginosa can induce the formation of small colony variants in S. In addition, positive interactions can also occur between microorganisms during polymicrobial infections. Besides active competition, regulatory effects induced for instance by the resident flora can induce the expression of important virulence and metabolic genes in P. Furthermore, recent results demonstrated that compounds such as phenazines inhibit methicillin-resistant S. aureus ( Lightbown and Jackson, 1954 Machan et al., 1992 Toder et al., 1994). aeruginosa to inhibit the cytochrome oxidase of S. aureus to obtain iron under iron-starvation conditions using LasA protease ( Mashburn et al., 2005), and 4-hydroxy-2-heptylquinoline N-oxide (HQNO) allows P. Bacterial interference occurs either via direct competition characterized by an active mechanism including the type VI secretion systems ( Pukatzki et al., 2006 Basler et al., 2013) and production of competitor molecules (siderophores, secondary metabolites, toxins), or via exploitative competition where one organism consumes the resources of another ( Cornforth and Foster, 2013 Boon et al., 2014). aeruginosa by competition and/or cooperation, determine the dynamics of lung colonization. Many ecological factors, including host immune responses as well as the presence of co-colonizing species interacting with P. The disappearance of the early colonizing species may be explained by antibiotic treatments or by competition between co-colonizing microorganisms. aeruginosa ( Folkesson et al., 2012) which progressively evolves toward a chronic colonization, that entails progressive lung tissue damage and impairment of pulmonary function. At the age of 20, 60–70% of CF-patients present intermittent colonization by P. predominate in older patients ( Goss and Burns, 2007 Cox et al., 2010 Lipuma, 2010). The composition of the microbial respiratory flora of cystic fibrosis (CF) patients changes with age Haemophilus influenzae and Staphylococcus aureus being present mainly in young children, while Pseudomonas aeruginosa, S. Manipulating these pathways could be used to interfere with bacterial interactions and influence the colonization by respiratory pathogens. aeruginosa and three other respiratory pathogens involving several major metabolic pathways. This work identified both detrimental and beneficial interactions occurring between P. coli.Ĭonclusion: Complex interactions take place between the various bacterial species colonizing CF-lungs. This growth defect could be restored either by addition of biotin or by co-culturing the mutant in the presence of K. We identified a beneficial interaction in a bioA transposon mutant, unable to grow on rich medium. This mutant displayed a severe growth deficiency in the presence of Gram-negative but not of Gram-positive bacteria. We further identified a transposon insertion in purF, encoding a key enzyme of purine metabolism. pneumoniae but not Escherichia coli and S. The carB mutant was also unable to grow in the presence of B. PqsC is involved in the synthesis of 4-hydroxy-2-alkylquinolines (HAQs), a family of molecules having antibacterial properties, while carB is a key gene in pyrimidine biosynthesis. aureus growth, two transposon insertions located in pqsC and carB, resulted in reduced growth inhibition. Results: Whereas wild-type PA14 inhibited S. aeruginosa genes required for exploitative and direct competitions with S. Methods: We generated a library of PA14 transposon insertion mutants to identify P. aeruginosa and other co-colonizing pathogens including Staphylococcus aureus, Burkholderia sp., and Klebsiella pneumoniae may be crucial for pathogenesis and disease progression. Background: Chronic airway infection by Pseudomonas aeruginosa considerably contributes to lung tissue destruction and impairment of pulmonary function in cystic-fibrosis (CF) patients.
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