According to new research, volatile compounds released by a bacterial pathogen called Pseudomonas aeruginosa can trigger the growth of a fungal pathogen often found in cystic fibrosis (CF) patients. This is the first time a study shows that a pathogen can send a signal through the air, acting as a direct fuel for another pathogen’s growth.
The findings were published recently in the journal mBio, an online open-access publication of the American Society for Microbiology (ASM), titled “Volatile Compounds Emitted by Pseudomonas aeruginosa Stimulate Growth of the Fungal Pathogen Aspergillus fumigatus.”
Both the P. aeruginosa bacteria and the Aspergillus fumigatus fungus are opportunistic pathogens, commonly found in the same region in the lungs’ microbiota. It has been shown that the bacteria can produce compounds that inhibit the growth of fungi, and since microbes tend to produce volatile compounds that can be airborne, Jean-Paul Latgé, Christoph Heddergott, and Benoit Briard – all members of the Pasteur Institute in Paris’ Aspergillus unit – wondered if these two pathogens would also communicate through volatile signals.
“To our big surprise, volatiles produced by Pseudomonas aeruginosa were promoting the growth of the Aspergillus fumigatus fungus,” Latgé said in an ASM press release. “Even more surprising, we found that these volatiles were actually taken up by the fungus to support growth.”
The team tested how these compounds would travel between the microbes by placing a small Petri dish of Aspergillus to one side inside a larger Petri dish of a Pseudomonas culture. Even separated by the two dishes, the microbes still shared the common airspace above the dishes’ surface.
“We simply put these two organisms together and in a couple of days, we were surprised to see the fungus growing faster and growing toward the bacteria,” Heddergott said. “This really indicated something stimulatory [coming from the bacteria].”
In order to find what could be triggering the growth, the team used particular types of fiber to absorb the volatile compounds that were being released from each pathogen to identify each one. Heddergott further tested every single volatile compound separately 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,” he said. Heddergott was then able to narrow his options down to just one airborne compound: dimethyl sulfide.
Since sulfur is such a vital component for the growth of Aspergillus, the researchers assessed if dimethyl sulfide was indeed being used as a food source by the fungus by placing the fungus on a food plate without sulfur and pumping dimethyl sulfide into the air. The team observed that the fungus grew with a significant added vitality when dimethyl sulfide was in the airspace.
“Before now, no one thought that a fungus could grow on volatile compounds bringing sulfur,” Latgé said, adding that this could explain why bacteria tend to colonize before fungus in the lungs in context of cystic fibrosis lung infections. “When the fungus reaches the patient’s lung, having bacteria that are releasing this volatile will help the fungus establish itself,” Latgé said.
The researchers said that understanding the links between these micro-organisms and how they colonize lungs may lead to improved prevention of bacterial-fungal infections, which are usually to blame for acute worsening of symptoms and decreased lung function among patients suffering from cystic fibrosis.
“This opens our eyes to look not at just a single organism in human infections, but rather a series of micro-organisms,” Latgé said. “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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