Jennifer Melinda Bomberger
Dartmouth College, NH·Microbiology & Immunology
People with cystic fibrosis (CF), an inherited disease that leaves thick, sticky mucus in the airways, often develop lung infections that last for years. The main cause is the bacterium Pseudomonas aeruginosa.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biochemistry
- Topics
Pseudomonas aeruginosa
cystic fibrosis
biofilm
- Grants
- 2 known grants, through Jan 2031
What they work on
- Test whether TsiT, a T6SS immunity protein that resembles LysR-type gene regulators, acts as a transcriptional regulator that controls Pseudomonas aeruginosa biofilm formation.
- Test whether TsiT-like genes in other Gram-negative bacteria, including Burkholderiales, protect those bacteria from TseT, a toxin that P. aeruginosa injects into competing cells through its type VI secretion system.
- Test how tsiT genes affect P. aeruginosa fitness during biofilm growth within a model cystic fibrosis airway microbial community.
- Determine how interferon-driven metabolic rewiring of the airway lining during RSV infection, including a shift toward aerobic glycolysis, supports viral-bacterial co-infection. The work will use human CF airway epithelial cell cultures and an RSV mouse model.
- Define how metabolites released by virus-infected airway cells promote P. aeruginosa persistence, both by weakening macrophage antibacterial function and by promoting bacterial biofilm growth.
More about the research
Over time it forms biofilms, which are slimy, protected bacterial communities that resist antibiotics, and these infections are a leading cause of illness and death in CF. This research asks what helps P. aeruginosa move from a short-term infection to a chronic one. One project looks at how the bacterium competes with neighboring microbes and controls its own biofilm growth. The other looks at how a viral infection in the host makes the airway more welcoming to the bacterium. Both projects use a specialized system that grows P. aeruginosa biofilms on human CF airway epithelial cells, the cells that line the airways.
Why it matters
P. aeruginosa infections are a leading cause of illness and death for people with cystic fibrosis, and its biofilms resist antibiotics. Explaining how a dual-role immunity protein, and the metabolic changes that viral infections cause, help the bacterium settle in for the long term could reveal new drug targets. Such targets might delay when patients first acquire the infection, or work alongside existing therapies to clear P. aeruginosa from the lungs.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniel J Wozniak
Ohio State University, OH·Microbiology & Immunology
Define how Psl, a secreted sugar polymer of Pseudomonas aeruginosa, suppresses Staphylococcus aureus growth and interacts with S. aureus protein A (SpA), using several complementary strategies.
Stephen Dolan
Clemson University, SC·Microbiology & Immunology·Early-career
Define the molecular basis of communication between Aspergillus fumigatus and Pseudomonas aeruginosa, mediated by the toxins gliotoxin and hydrogen cyanide, by co-culturing them in synthetic cystic fibrosis sputum.
Muhammad Zafar
Emory University, GA·Microbiology & Immunology
Determine the distinct roles of the two genetically separate ethanolamine utilization (eut) gene clusters of Klebsiella pneumoniae in using ethanolamine, a membrane and diet byproduct, as a nutrient in the mouse gut.
The school
Dartmouth College: 16 labs on PI Pages, $418M a year on research, 104 research doctorates a year.
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