Volatile compounds released by the bacteria Pseudomonas aeruginosa fuel the growth of a fungal pathogen found in lung infections in cystic fibrosis (CF) patients, according to a study recently published in the American Society for Microbiology (ASM) journal mBio.
The study, “Volatile Compounds Emitted by Pseudomonas aeruginosa Stimulate Growth of the Fungal Pathogen Aspergillus fumigatus,” is the first to show that one pathogen can emit an airborne signal that directly fuels the growth of another pathogen.
Pseudomonas aeruginosa is the most frequently colonizing bacterium in CF patients, and it is often found in association with the filamentous fungus Aspergillus fumigatus. Previous research has shown that when the two pathogens come into direct contact, the bacteria produces compounds that inhibit fungal growth.
Emerging studies have shown that communication between microbial species involves not only water-soluble compounds, but also the release and detection of volatile organic compounds (VOCs). Recent and ongoing work has emphasized the role of microbial communication via gas phase VOCs, and repeatedly reported their inhibition of fungal growth.
Based on the evidence, Benoit Briard, Christoph Heddergott, and Jean-Paul Latgé at the Pasteur Institute in Paris, wondered if Pseudomonas aeruginosa and the fungus Aspergillus fumigatus could also communicate via volatile signals.
“To our big surprise, volatiles produced by Pseudomonas aeruginosa were promoting the growth of the Aspergillus fumigatus fungus,” said Dr. Latgé in an ASM news release. “Even more surprising, we found that these volatiles were actually taken up by the fungus to support growth.”
To examine how volatile compound signals might travel and influence the microbes, the researchers used Petri dishes and placed Aspergillus in one dish and a Pseudomonas culture in another. “We simply put these two organisms together and in a couple of days, we were surprised to see the fungus growing faster and growing towards the bacteria,” Dr. Heddergott said. “This really indicated something stimulatory [coming from the bacteria].”
Researchers investigated the mechanism behind this by using special fibers to absorb the volatile compounds released from each microbe. They then examined each of the VOCs produced by Pseudomonas individually on the fungus alone.
“The most stinky ones containing sulfur stimulated the fungus to grow at the same concentration as co-growing with the bacteria,” Dr. Heddergott said. Further work narrowed the airborne compounds down to one mainly responsible for growth — dimethyl sulfide.
Aspergillus needs sulfur to grow, so the researchers examined if dimethyl sulfide was serving as a nutritious source. The team placed the fungus on a plate of food absent of sulfur, and then pumped dimethyl sulfide into the air. They found the fungus grew better with the presence of dimethyl sulfide, and collected dimethyl sulfide directly from the air.
“Before now, no one thought that a fungus could grow on volatile compounds bringing sulfur,” Dr. Latgé said, adding that, in CF, this finding could explain why bacteria usually colonize lungs first, followed by fungus. “When the fungus reaches the patient’s lung,” he said, “having bacteria that are releasing this volatile will help the fungus establish itself.”
The study unexpectedly showed that human opportunistic pathogens can interact at a distance after sensing volatiles emitted by another microbial species. The finding opens a new research avenue for the understanding of microbial communities, which are responsible for the deterioration of lung function in CF patients.
“This opens our eyes to look not at just a single organism in human infections, but rather a series of microorganisms,” concluded Dr. Latgé. “They can be far away from each other, communicating over a distance, and even using volatile compounds produced by another microbe to grow.”
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