Daniel Voth
University of Arkansas for Medical Sciences, AR·Microbiology & Immunology
Q fever, caused by the bacterium Coxiella burnetii, usually looks like the flu but can turn into chronic endocarditis, a potentially fatal infection of the heart. Treatment for Q fever endocarditis works poorly and requires many months of antibiotics.
- Fields
Microbiology & Immunology
Pharmacology
Medicine & Clinical Research
- Topics
Coxiella burnetii
Q fever
endocarditis
- Grants
- 1 known grant, through Apr 2027
What they work on
- Identify which neurotransmitter signaling machinery in human alveolar macrophages Coxiella burnetii needs to replicate, using host-directed drugs that block these pathways.
- Determine whether neurotransmitter-acting drugs prevent C. burnetii from dampening the cytokine response and shifting lung macrophages to an anti-inflammatory state that favors bacterial growth.
- Test the effects of these drugs on infection in primary human alveolar macrophages and human precision-cut lung slices, thin sections of living lung tissue, to assess disease relevance.
More about the research
One alternative is to target the host rather than the microbe. The team recently found that several drugs normally used for psychosis or mood disorders, which block neurotransmitter signaling, suppress C. burnetii growth inside human macrophages, the immune cells the bacterium infects.
Why it matters
Patients with chronic Q fever endocarditis currently have no effective treatment beyond months of largely ineffective antibiotics. Characterizing how existing psychiatric drugs that act on neurotransmitter signaling suppress Coxiella burnetii in human lung immune cells could identify them as candidate host-directed therapies for Q fever.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Christina Leigh Stallings
Washington University in St Louis, MO·Microbiology & Immunology
Define how SPTLC2, the rate-limiting enzyme subunit for building sphingolipids, supports maintenance and monocyte-derived repopulation of alveolar macrophages during M. tuberculosis infection, using mice lacking Sptlc2 in CD11c+ lung cells.
Avishek Mitra
Oklahoma State University, OK·Microbiology & Immunology
Determine how Rv0125, a protein Mtb releases outside the cell, strips heme from host hemoproteins such as hemoglobin, and whether it is a shared core component of the bacterium's heme uptake routes.
Amariliz Rivera
Rutgers University-New Brunswick, NJ·Microbiology & Immunology
Compare how tissue-derived and monocyte-derived alveolar macrophages, two lung immune-cell groups with different origins, reduce pathogen burden and protect lung tissue during helminth, fungal and viral infections, using discovery-based and targeted in vitro and in vivo studies.
The school
University of Arkansas for Medical Sciences: 7 labs on PI Pages, $227M a year on research, 40 research doctorates a year.
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