Research

The Hunter lab uses ecological approaches to define the environmental chemistry of the airways, understand how microbes adapt, and how to manipulate this niche to slow disease development.

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Nutrient acquisition by respiratory pathogens

Nutrient sources that sustain bacterial growth in the respiratory tract, and how those nutrients are derived, are not well characterized. Our lab is defining the microbe-microbe and host-microbe interactions that sustain the bioavailable carbon budget in the infected respiratory tract, and the metabolic strategies respiratory pathogens use to obtain these resources. Airway mucins represent an abundant nutrient source within the airways. The lab works to understand the process of mucin degradation by both anaerobic bacterial communities and the host, as well as its role in providing a nutritional landscape that can support the growth of opportunistic pathogens in the airways.

 
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Translational activity of CF microbiota

To characterize the in situ ecophysiology of microbial communities in the CF airways, our lab uses bioorthogonal non-canonical amino acid tagging (BONCAT), a ‘click’ chemistry-based metabolic labeling approach. BONCAT results in a fluorescently labeled population of translationally active cells that can be further studied with high-resolution imaging, genomics, proteomics and a variety of other analytical tools.

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Achromobacter xylosoxidans

Achromobacter xylosoxidans is recognized as an emerging multi-drug resistant pathogen in patients with cystic fibrosis, colonizing anywhere from 2 to 20 percent of CF subjects. Relative to other canonical CF pathogens, little is known about the physiology and molecular biology of A. xylosoxidans and its role in pathogenesis. Our lab is using various methods of genetic manipulation and airway infection models to determine genetic factors contributing to infection, proliferation, and persistence of this bacterium.

 
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Microbial ecology of chronic rhinosinusitis

Bacterial sinusitis affects more than 15% of the population, though the microbiology of this disease remains poorly understood. Recent 16S sequencing efforts have implicated a number of suspected pathogens, but bacterial metabolic strategies and their specific contributions to upper airway disease are not yet known. We utilize a combination of single cell imaging, proteomics, and chemical measurements (pH, O2, nutrient sources) to characterize the ecological dynamics of chronic sinus infections.