A new study led by the team of scientists from the University of Notre Dame and the University of Illinois at Urbana-Champaign has found a new defense mechanism used by the bacterium, Pseudomonas aeruginosa to communicate in groups to avoid antibiotics.
Pseudomonas aeruginosa is a pathogen causing diseases like pneumonia, sepsis and other infections. On an encounter with antibiotics, pathogen produces a signal to develop protective behaviors that contribute to its ability to tolerate some antibiotics.
“There is a general lack of understanding about how communities of bacteria, like the opportunistic pathogen P. aeruginosa, respond to antibiotics,” said Nydia Morales-Soto, the senior research scientist in civil and environmental engineering and earth sciences (CEEES) at the University of Notre Dame and lead author of the paper. “Most of what we know is from studies about stationary biofilm communities, whereas less is known about the process beforehand when bacteria are colonizing, spreading and growing. In this study, our research team specifically reviewed the behavior of bacteria during this period and what that may mean for antibiotic resistance.”
During their research, researchers found that when antibiotic was smeared to a colony of P. aeruginosa, a Pseudomonas quinolone signal (PQS) were produced by the bacteria in its surrounding. They also produced secondary signals, known as the alkyl hydroxyquinoline (AQNO).
After this, the next step of the team was to determine the response. To determine this, they mapped production of each response spatially and found out that P. aeruginosa is capable of producing PQS in small pockets at significantly higher concentrations than previously recorded.
The study revealed that PQS and AQNO are independently regulated responses that are intentionally communicating different messages. Additionally, this means the bacteria type may have some capability to protect the colony from some external toxins while the bacteria are still in a colonizing phase.
“Although the AQNO response identified in the paper is a stress-dependent behavior, it is such a new chemical message that it has not yet been definitively labeled as a signal. Although based on our findings, we believe it is,” said Joshua Shrout, associate professor of CEEES and concurrent associate professor of biological sciences at the University of Notre Dame and co-author of the paper.
“Regardless, this work opens a new window into understanding P. aeruginosa behavior and potentially how this bacterium promotes tolerance to antibiotics.”
