Microbe Wars: Benign oral bacterium represses major cystic fibrosis pathogen

Microbe Wars: Benign oral bacterium represses major cystic fibrosis pathogen

Pseudomonas aeruginosa is a bacterium that can cause devastating lung infections in cystic fibrosis patients. It lives with multiple other microbes in biofilms in these patients’ airways, and is resistant to many antibiotics. Hui Wu and colleagues at the University of Alabama at Birmingham have been investigating microbial behavior in these biofilms, resulting in some surprising findings. I interviewed Wu via email to find out more.

Hui WuDr. Wu, you work in the School of Dentistry at the University of Alabama at Birmingham. What led you to study microbial biofilms, and how do they relate to dentistry research?

HW: Hundreds and thousands of microbes reside in your mouth, forming sticky films called oral biofilms, also known as dental plaque. These biofilms can cause tooth decay and gum disease, infections which are also associated with systemic conditions like cardiovascular disorders and cancers. This is why it is important to keep your mouth clean by brushing or flossing.

Do you have a “favorite” microbe?

HW: Our favorite microbe, Streptococcus parasanguinis, is the most abundant streptococcus in the oral cavity, according to the National Institutes of Health-sponsored Human Microbiome Project. We have discovered it is a probiotic-like organism that can kill many gram-negative pathogens while maintaining itself.

Tell us about the effect microbes have in cystic fibrosis patients? Why should we be looking beyond Pseudomonas aeruginosa to understand pulmonary infections?

HW: Microbial infections often kill cystic fibrosis patients. Pseudomonas aeruginosa has been recognized as a major pathogen in these patients; however, recent microbiome studies have revealed that the presence of oral commensal streptococci may improve disease outcomes. A better understanding of microbial activities may therefore point to new therapeutic targets or approaches to combat this devastating infection.

In your study, you found that S. parasanguinis may interfere with P. aeruginosa pathogenicity within a biofilm. What have you discovered about the mechanism by which this interaction occurs?

HW: The finding is unexpected and stunning. On the one hand, S. parasanguinis seems to cooperate with P. aeruginosa: two surface-exposed streptococcal molecules seem to encourage P. aeruginosa to produce extracellular matrix, which supports the streptococcus biofilm. On the other hand, S. parasanguinis represses mucoid P. aeruginosa – a dramatic twist. This new dynamic speaks to the complexity of microbial interactions, which may lead to new opportunities to control bacterial infections.

The reduction in P. aeruginosa pathogenicity that streptococci appear to bring about may be beneficial for humans, but what is the evolutionary benefit to the streptococci?

HW: The streptococcus is the biggest winner in this situation: it likely outcompetes many other pathogens, even the notoriously pathogenic P. aeruginosa, using its biofilm as a fortified base. Mucoid P. aeruginosa has evolved to shield itself from the bombardment of antibiotics, but in S. parasanguinis, we have found an astonishing secret weapon. Whether P. aeruginosa can ultimately overcome such attack is an interesting direction for further investigation.

What do your results mean for our wider understanding of how diverse microbes interact within our bodies, and how should this affect how we study microbial disease?

HW: Microbial interactions are context dependent. They are dynamic and complex, and driven by multiple factors. Therefore, when we study microbial interactions, we need to take holistic approaches to uncover a more complete picture of microbial pathogenesis.

What impact do you hope your study might have in your field, and what are the next steps for your research?

HW: The interaction we uncovered here is just the tip of the iceberg in microbe-host interactions. We hope further research will examine dynamic microbial interactions using “omics” and big data approaches. There are two questions we can address now. Firstly, what are the additional tools that S. parasanguinis employs to exploit harmful products made by P. aeruginosa? Secondly, could S. parasanguinis act as a probiotic to treat chronic P. aeruginosa infection in cystic fibrosis patients?

 

Research Article: Scoffield JA, Duan D, Zhu F, Wu H (2017) A commensal streptococcus hijacks a Pseudomonas aeruginosa exopolysaccharide to promote biofilm formation. PLoS Pathog 13(4): e1006300. https://doi.org/10.1371/journal.ppat.1006300

Images Credits: adrigu, Flickr; Hui Wu

Author

Beth works at PLOS as Journal Media Manager. She read Natural Sciences, specializing in Pathology, at the University of Cambridge before joining PLOS in 2013. She feels fortunate to be able to read and write about the exciting new research published by PLOS.

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