Genetic adaptation by Pseudomonas aeruginosa to the airways of cystic fibrosis patients.

By E. Smith, D. Buckley, Zaining Wu, C. Saenphimmachak, L. Hoffman, David A. D'Argenio, Samuel I. Miller, B. Ramsey, D. Speert, S. Moskowitz and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2006

1,392 citations recorded by the source corpus.

Subfields: Molecular Biology, Molecular Medicine, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/93e95336a2135690d75a8fdb38ecf23845df0ccf

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Citations in the corpus

Lipopolysaccharide modification in Gram-negative bacteria during chronic infection. (2016, background): “…et al. , 2005), reduced expression of virulence factors, which is presumably an adaptive strategy to escape detection by the host immune system (Smith et al. , 2006), increased activity of efflux pumps associated with antibiotic resistance, especially against those antibiotics used clinically…”
De novo bacterial genome sequencing: millions of very short reads assembled on a desktop computer. (2008, methodology): “These two new data sets were then assembled with the Minimus assembler (Sommer et al. 2007), as shown in Table 2.”
The hierarchy quorum sensing network in Pseudomonas aeruginosa (2014, background): “…functions of the central las system (Lee et al., 2013), providing critical clues in understanding the puzzling phenomenon that the clinical isolates of P. aeruginosa frequently harbour mutated lasI or lasR genes (Ciofu et al., 2010; D’Argenio et al., 2007; Hoffman et al., 2009; Smith et al., 2006).”
Genomic analysis reveals that Pseudomonas aeruginosa virulence is combinatorial (2006, background): “Indeed, a recent comparison of an early and late CF isolate from the same patient (at 6 months and 8 years of age) revealed an accumulation of multiple mutations leading to gene inactivation or loss, including a large 188 kb deletion [ 33 ].”
Pseudomonas aeruginosa: new insights into pathogenesis and host defenses. (2013, background): “aeruginosa isolated from acute infections differ substantially in phenotype from those isolated from chronic infections (Smith et al., 2006).”
Pseudomonas aeruginosa Evolutionary Adaptation and Diversification in Cystic Fibrosis Chronic Lung Infections (2016, background): “In particular, there have been a number of studies reporting comparisons of clonally related longitudinal isolates, mostly contrasting the mutated genes in isolates from early and late in the infection process [24–29].”
Bacterial quorum sensing: its role in virulence and possibilities for its control. (2012, background): “A potential complication in targeting LasR is that, as mentioned, some clinical P. aeruginosa isolates possess defective LasR proteins (Smith et al. 2006).”