Jon E. Paczkowski, PhD
Health Research Inc., New York State Department of Health
Research Project:
Characterization of the Effects of Microbial Adaptation to Understand Quorum Sensing Progression in Pathogenesis
Grant Awarded:
- Innovation Award
Research Topics:
- basic biologic mechanisms
- gene expression transcription
- public health
Research Diseases:
- asthma
- COPD
- cystic fibrosis
- lung cancer
- pneumonia
- pulmonary fibrosis
The disease-causing bacteria Pseudomonas aeruginosa uses a cell-cell communication process called quorum sensing to orchestrate collective behaviors required for disease development. Quorum sensing relies on the group-wide detection of signal molecules called autoinducers. The production and detection of autoinducers are required for disease development. A bacterial infection is not a static event; bacteria must first colonize inside the body, then proliferate and survive within the body, and eventually transfer into another person. Since conditions within the body are different than outside, and conditions within the body might change during the course of the infection, microbial adaptation is key to the infection process to ensure the survival of the bacteria. We will examine the role of microbial adaption in altering autoinducer concentrations to modulate disease-developing traits of Pseudomonas aeruginosa. This will help us to better understand how we could potentially block cell-cell signaling to prevent disease development.
Update:
We studied how three changes in amino acids affect a protein that makes autoinducers. This starts a process responsible for turning on of disease-causing traits. We found that strains with these changed amino acids make more harmful traits compared to other types. We detected and analyzed the levels of autoinducers made by these variant strains. We found that these variants optimally adjust autoinducer levels, making harmful traits increase. We think these variants enhance the fitness of P. aeruginosa in people because they improve quorum sensing to drive the timely expression of genes involved in disease development.
Page last updated: September 17, 2024
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