Postdoc Spotlight: Kaitlyn Whitefoot-Keliin

Kaitlyn Whitefoot-Keliin is a postdoctoral fellow in the Lawrenz lab within the department of Microbiology and Immunology in the School of Medicine. She earned her PhD in Biochemistry, Cell and Molecular Biology from Central Michigan University.

Could you tell us about this work and how this achievement will impact your professional career?

"I recently received an NIH National Institute of Allergy and Infectious Diseases (NIAID) NRSA F32 Postdoctoral Fellowship, which will support my research on how Yersinia pestis, the bacterium that causes plague, manipulates host inflammatory responses to promote infection. One of the most intriguing features of plague is that, unlike many bacterial infections that provoke a rapid inflammatory response, infection begins in a largely non-inflammatory environment despite extensive bacterial replication before progressing to severe inflammation later in disease. My research seeks to understand the mechanisms that drive this transition and how Y. pestis reshapes the host environment to establish infection.

This fellowship represents an important step in my development as an independent scientist. During my doctoral training, I studied how small particles called extracellular vesicles are altered during bacterial infection and how they contribute to coagulation and inflammation. Through the F32, I am extending those interests into new questions centered on how Y. pestis reshapes the inflammatory environment to promote infection. Although the pathogen and experimental approaches are different, my research has remained focused on understanding how inflammation is regulated during infection and how it contributes to disease.

In addition to supporting this research, the fellowship will provide the time and resources needed to pursue these questions while continuing my development as an independent scientist. It will also help prepare me for the transition from postdoctoral training to an independent research career."

What is your research about?

"My research focuses on understanding how Y. pestis manipulates host inflammatory responses to promote infection. The focus of my F32 fellowship is to determine how prostaglandin E2 (PGE₂) influences host immunity during plague. While PGE₂ is a well-studied regulator of inflammation, its effects are highly dependent on biological context, and its role during Y. pestis infection remains poorly understood. Interestingly, PGE₂ is produced early during infection, raising important questions about why it is generated at this stage and what role it serves in shaping the host response. Whether PGE₂ functions to suppress inflammation, protect host tissues, or regulate other aspects of immunity remains unclear. My work seeks to determine how PGE₂ synthesis is regulated and whether its early production influences disease progression. 

I also investigate leukotriene B4 (LTB₄), a well-established inflammatory lipid mediator that promotes immune cell recruitment and activation. While the general functions of LTB₄ are defined, its specific role during Y. pestis infection remains incompletely understood. Studying both PGE₂ and LTB₄ allows me to examine how distinct lipid pathways are regulated throughout infection and how they contribute to disease progression. As part of these studies, I use spatial transcriptomics to define how PGE₂ and LTB₄ signaling shape the transcriptional landscape of the infected lung. This approach allows me to examine how inflammatory lipid signaling influences local immune responses and the development of inflammation. It is also helping me define the transcriptional programs associated with direct bacterial interaction and determine how they differ from responses in surrounding bystander cells. This distinction is important because cells that directly encounter the bacterium may respond very differently from neighboring cells that are exposed only to the surrounding inflammatory environment. Together, these studies aim to understand how lipid-mediated signaling shapes the balance between protective immunity and inflammation during Y. pestis infection. Ultimately, this work may identify new therapeutic strategies for bacterial pneumonia."

What are your career goals and vision?

"My long-term goal is to establish an independent academic research program focused on microbial pathogenesis and infection-associated inflammation. What excites me most about this area of research is understanding how bacteria reshape the host environment to their advantage and identifying the mechanisms that determine whether a host response is protective or permissive to infection. Throughout my training, I have been drawn to questions that seek to understand how bacteria establish permissive immune environments that allow infection to progress despite the presence of host defenses. These questions continue to shape the direction of my research and the type of scientific program I hope to build as an independent investigator, particularly as emerging and re-emerging pathogens continue to highlight the need for a deeper understanding of host-pathogen interactions.

Equally important to my long-term goals is mentorship. Discoveries made today are only part of a researcher's legacy; the scientists we train will continue to shape science long after our own careers. Mentoring students has been one of the most rewarding aspects of my training, and it has reinforced my commitment to helping young scientists develop the skills and confidence needed to pursue their own scientific questions. I hope to train researchers who are not only technically skilled, but also capable of thinking creatively and tackling the complex scientific problems that will define the future of infectious disease research."

If you are a postdoc at UofL and want to share your accomplishments, email us at ulpda@louisville.edu.