Research Interests

In our lab, we want to understand how bacteria thrive within the very cells that are meant to eliminate them. We use Legionella pneumophila, the bacterium that causes Legionnaires’ disease, to explore how pathogens reshape host cells and build protected niches, revealing new connections between infection biology and the cell’s normal defenses.

We are especially interested in how bacterial effector proteins find their way to host membranes and interact with the cell’s regulatory machinery. We study phosphoinositides, the lipids that help define membrane identity, alongside host GTPases, cytoskeletal regulators, and host signaling adaptors. These interactions offer a window into how bacteria redirect membrane traffic and organize their surroundings from the moment they enter a host cell.

We also explore how infection changes mitochondrial organization, autophagy, and protein quality control, and how these changes affect bacterial survival and host defense. An emerging interest is whether changing host metabolic pathways can help macrophages clear intracellular bacteria while preserving cell function. Through collaborative work on bacterial cell-wall recycling, we also explore how bacteria sustain themselves inside macrophages. Our team combines microbial genetics, protein biochemistry, quantitative imaging, proteomics, and structural analysis to uncover general principles of host-pathogen interactions and identify vulnerabilities that could inform future host-directed and anti-virulence strategies.
 

Current Projects

Both amoebae and macrophages are phagocytic cells and they engulf and destroy microorganisms. Under normal circumstances, the phagosome containing the cargo destined for degradation undergoes maturation through sequential fusion with endocytic compartments and ultimately with the lysosome to destroy its contents. However,  L. pneumophila resists degradation in both cell types by blocking phagosome maturation. A current focus in our lab is to determine how L. pneumophila modulates membrane transport pathways of the host cell to derail phagosome maturation.

A striking feature of L. pneumophila is its ability to translocate a vast number of effector proteins into the host cell to subvert the function of key regulatory proteins including Rab GTPases. These proteins act as molecular switches and they are attractive targets for intracellular bacterial pathogens due to the pivotal roles they play in eukaryotic cell function. Rab GTPases are targeted by L. pneumophila effector proteins during infection and our group is pursuing the mechanisms that L. pneumophila uses to manipulate their activity. We focus on determining how L. pneumophila effector proteins control the activity of host small GTPases through post-translational modifications. 
 

Research Group

Graduate students

• Samual Allgood (doctoral)
• Rebecca Noll (doctoral)
• Colleen Pike (doctoral)
• Barbara Romero-Dueñas (doctoral)

Undergraduate students

• Andre Cunningham
• Matthew Bott
   

Education

• B.A., M.S. - Babes-Bolyai University (Romania)
• Ph.D. -  Texas A&M University
• Postdoctoral - National Institute for Child Health and Human Development, National Institutes of Health
  
  

Teaching

• BISC 300 - Introduction to Microbiology
• BISC 850 - Advanced Topics in Host-Microbe Interaction