Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Mar 18;22(6):3128.
doi: 10.3390/ijms22063128.

Pseudomonas aeruginosa: An Audacious Pathogen with an Adaptable Arsenal of Virulence Factors

Affiliations
Review

Pseudomonas aeruginosa: An Audacious Pathogen with an Adaptable Arsenal of Virulence Factors

Irene Jurado-Martín et al. Int J Mol Sci. .

Abstract

Pseudomonas aeruginosa is a dominant pathogen in people with cystic fibrosis (CF) contributing to morbidity and mortality. Its tremendous ability to adapt greatly facilitates its capacity to cause chronic infections. The adaptability and flexibility of the pathogen are afforded by the extensive number of virulence factors it has at its disposal, providing P. aeruginosa with the facility to tailor its response against the different stressors in the environment. A deep understanding of these virulence mechanisms is crucial for the design of therapeutic strategies and vaccines against this multi-resistant pathogen. Therefore, this review describes the main virulence factors of P. aeruginosa and the adaptations it undergoes to persist in hostile environments such as the CF respiratory tract. The very large P. aeruginosa genome (5 to 7 MB) contributes considerably to its adaptive capacity; consequently, genomic studies have provided significant insights into elucidating P. aeruginosa evolution and its interactions with the host throughout the course of infection.

Keywords: Pseudomonas aeruginosa; adaptation; cystic fibrosis; diversity; genomics; lung environment; virulence factors.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the writing of the manuscript, or in the content of the review.

Figures

Figure 1
Figure 1
Schematic presentation of the main virulence factors used by P. aeruginosa during respiratory infections: (a) biofilm formation ability and composition of the extracellular matrix of biofilms (exopolysaccharides, proteins and extracellular DNA); (b) the three main quorum sensing (QS) systems (Las, Rhl and Pqs); (c) flagellins FliC and FliD incorporated within the flagellar structure; (d) pyoverdine (PVD) siderophore as an iron uptake system; (e) type 4 pili (T4P); (f) lipopolysaccharide (LPS) and outer membrane proteins (OMPs); (g) the type III secretion system (T3SS) and its four main effectors; (h) the type VI secretion system (T6SS); (i) the type II secretion system (T2SS) and the compounds it releases to the extracellular milieu: lytic enzymes (lipases, proteases (AprA ad PIV) and elastases (LasA and LasB)), exotoxin A (ETA), and pyocyanin.
Figure 2
Figure 2
Representation of P. aeruginosa adaptation to the cystic fibrosis (CF) lung over the course of infection. In early stages, isolates are fully equipped with virulence factors that allow respiratory tract colonisation and lung injury. The stressful environment of the CF airway drives P. aeruginosa pathoadaptative changes that enable long-term colonisation and establishment of recalcitrant infections.

References

    1. Riquelme S.A., Liimatta K., Wong Fok Lung T., Fields B., Ahn D., Chen D., Lozano C., Sáenz Y., Uhlemann A.C., Kahl B.C., et al. Pseudomonas aeruginosa Utilizes Host-Derived Itaconate to Redirect Its Metabolism to Promote Biofilm Formation. Cell Metab. 2020;31:1091–1106. doi: 10.1016/j.cmet.2020.04.017. - DOI - PMC - PubMed
    1. Fernández-Barat L., Ferrer M., De Rosa F., Gabarrús A., Esperatti M., Terraneo S., Rinaudo M., Li Bassi G., Torres A. Intensive care unit-acquired pneumonia due to Pseudomonas aeruginosa with and without multidrug resistance. J. Infect. 2017;74:142–152. doi: 10.1016/j.jinf.2016.11.008. - DOI - PubMed
    1. Wunderink R.G., Waterer G. Advances in the causes and management of community acquired pneumonia in adults. BMJ. 2017;358:j2471. doi: 10.1136/bmj.j2471. - DOI - PubMed
    1. Garcia-Nuñez M., Marti S., Puig C., Perez-Brocal V., Millares L., Santos S., Ardanuy C., Moya A., Liñares J., Monsó E. Bronchial microbiome, PA biofilm-forming capacity and exacerbation in severe COPD patients colonized by P. aeruginosa. Future Microbiol. 2017;12:379–392. doi: 10.2217/fmb-2016-0127. - DOI - PubMed
    1. Winstanley C., O’Brien S., Brockhurst M.A. Pseudomonas aeruginosa Evolutionary Adaptation and Diversification in Cystic Fibrosis Chronic Lung Infections. Trends Microbiol. 2016;24:327–337. doi: 10.1016/j.tim.2016.01.008. - DOI - PMC - PubMed

Substances