Anaerobic Metabolism by Pseudomonas aeruginosa in Cystic Fibrosis Airway

2004 ◽  
pp. 97-118
2008 ◽  
Vol 21 (4) ◽  
pp. 595-599 ◽  
Author(s):  
Sophie Moreau-Marquis ◽  
Bruce A. Stanton ◽  
George A. O’Toole

2006 ◽  
Vol 103 (48) ◽  
pp. 18131-18136 ◽  
Author(s):  
H. Matsui ◽  
V. E. Wagner ◽  
D. B. Hill ◽  
U. E. Schwab ◽  
T. D. Rogers ◽  
...  

2012 ◽  
Vol 10 (12) ◽  
pp. 841-851 ◽  
Author(s):  
Anders Folkesson ◽  
Lars Jelsbak ◽  
Lei Yang ◽  
Helle Krogh Johansen ◽  
Oana Ciofu ◽  
...  

2008 ◽  
Vol 190 (8) ◽  
pp. 2739-2758 ◽  
Author(s):  
Mark D. Platt ◽  
Michael J. Schurr ◽  
Karin Sauer ◽  
Gustavo Vazquez ◽  
Irena Kukavica-Ibrulj ◽  
...  

ABSTRACT Patients suffering from cystic fibrosis (CF) commonly harbor the important pathogen Pseudomonas aeruginosa in their airways. During chronic late-stage CF, P. aeruginosa is known to grow under reduced oxygen tension and is even capable of respiring anaerobically within the thickened airway mucus, at a pH of ∼6.5. Therefore, proteins involved in anaerobic metabolism represent potentially important targets for therapeutic intervention. In this study, the clinically relevant “anaerobiome” or “proteogenome” of P. aeruginosa was assessed. First, two different proteomic approaches were used to identify proteins differentially expressed under anaerobic versus aerobic conditions. Microarray studies were also performed, and in general, the anaerobic transcriptome was in agreement with the proteomic results. However, we found that a major portion of the most upregulated genes in the presence of NO3 − and NO2 − are those encoding Pf1 bacteriophage. With anaerobic NO2 −, the most downregulated genes are those involved postglycolytically and include many tricarboxylic acid cycle genes and those involved in the electron transport chain, especially those encoding the NADH dehydrogenase I complex. Finally, a signature-tagged mutagenesis library of P. aeruginosa was constructed to further screen genes required for both NO3 − and NO2 − respiration. In addition to genes anticipated to play important roles in the anaerobiome (anr, dnr, nar, nir, and nuo), the cysG and dksA genes were found to be required for both anaerobic NO3 − and NO2 − respiration. This study represents a major step in unraveling the molecular machinery involved in anaerobic NO3 − and NO2 − respiration and offers clues as to how we might disrupt such pathways in P. aeruginosa to limit the growth of this important CF pathogen when it is either limited or completely restricted in its oxygen supply.


PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16246 ◽  
Author(s):  
Matthew L. Mayer ◽  
Jared A. Sheridan ◽  
Christoph J. Blohmke ◽  
Stuart E. Turvey ◽  
Robert E. W. Hancock

Antibiotics ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 827
Author(s):  
Emma Reece ◽  
Pedro H. de Almeida Bettio ◽  
Julie Renwick

Pseudomonas aeruginosa is one of the most dominant pathogens in cystic fibrosis (CF) airway disease and contributes to significant inflammation, airway damage, and poorer disease outcomes. The CF airway is now known to be host to a complex community of microorganisms, and polymicrobial interactions have been shown to play an important role in shaping P. aeruginosa pathogenicity and resistance. P. aeruginosa can cause chronic infections that once established are almost impossible to eradicate with antibiotics. CF patients that develop chronic P. aeruginosa infection have poorer lung function, higher morbidity, and a reduced life expectancy. P. aeruginosa adapts to the CF airway and quickly develops resistance to several antibiotics. A perplexing phenomenon is the disparity between in vitro antimicrobial sensitivity testing and clinical response. Considering the CF airway is host to a diverse community of microorganisms or ‘microbiome’ and that these microorganisms are known to interact, the antimicrobial resistance and progression of P. aeruginosa infection is likely influenced by these microbial relationships. This review combines the literature to date on interactions between P. aeruginosa and other airway microorganisms and the influence of these interactions on P. aeruginosa tolerance to antimicrobials.


Sign in / Sign up

Export Citation Format

Share Document