Although we primarily study bacteria using pure planktonic culture approaches in the lab, observations dating back as early as the 17th century have shown that microbes can adopt a biofilm lifestyle composed of multiple species.
This dichotomy between how we study microbes in the lab compared to how they grow in the environment may introduce a potential bias in our understanding of microbial physiology, particularly in the context of infections (e.g., cystic fibrosis, chronic wounds, etc.).
Therefore, the long-term goal of my group is to understand the molecular mechanisms driving changes in bacterial phenotypes when grown as polymicrobial biofilm-like communities. Such approaches will ultimately lead to development of new strategies to eradicate these recalcitrant biofilms.
Several microbial-based human infections (periodontitis, respiratory diseases, chronic wounds, etc.) are exacerbated by the presence of polymicrobial communities. More alarmingly, conventional treatment strategies based on a "one microbe, one disease" approach oftentimes fail to eradicate such complex biofilms observed during disease. Therefore, we are approaching a bottleneck in our ability to treat these infections using currently available antimicrobial-based approaches. We argue that identifying and characterizing the mechanisms driving the recalcitrance of such polymicrobial biofilms could represent novel therapeutic targets.
To achieve this, we use cystic fibrosis (CF) as a chronic and polymicrobial-based airway infection model. CF is a hereditary genetic disease affecting over 100,000 individuals worldwide and impacting multiple organs, particularly the respiratory tract. The lungs of these individuals are colonized by several pathogens, including Pseudomonas aeruginosa, Staphylococcus aureus, streptococci, and various Prevotella species.
Through in vitro modeling of polymicrobial communities, we study the mechanisms whereby these microbes exhibit altered susceptibility to front-line clinical antimicrobial agents (PMID: 33727344; PMID: 36661299).
One of the goals of my lab is to develop new experimental model systems to study microbial phenotypes in a polymicrobial context. To achieve this, we aim at leveraging various data sets/studies to guide our modeling efforts. Such models are critical to explore at the molecular level, emerging microbial phenotypes that may not be observed using pure bacterial cultures (PMID: 33727344; PMID: 33681294; PMID: 38709077). Ultimately, such systems will help generate new molecular knowledge and potentially lead to positive impacts on human and environmental health.
In the long term, we seek to develop innovative therapeutic approaches against polymicrobial biofilms observed during infections. Thus, my lab focuses on identifying molecules that exhibit unexpected activity against bacteria living in multi-species communities (PMID: 33727344).