Medicine Insider sat down to learn a little more about Phillip West, Ph.D., assistant professor in the Department of Microbial Pathogenesis and Immunology. Dr. West’s laboratory employs a diverse array of cell and animal models to investigate how mitochondria regulate innate immunity and inflammatory responses during infection, metabolic diseases, and cancer. His group is currently exploring the signaling pathways linking mitochondria to innate immunity with the ultimate goal of defining how these pathways modulate host responses to intracellular pathogens and influence the pathobiology of mitochondrial disorders and inflammatory diseases. The West lab is also examining how mitochondrial genome instability modulates innate and adaptive immunity in the melanoma microenvironment to shape anti-tumor immune responses.
Dr. West received dual B.S. degrees in Biology and Science Education in 2001 from North Carolina State University. He then worked as laboratory technician in the Department of Microbiology and Immunology at Wake Forest University School of Medicine for three years before pursuing his doctorate degree at Yale School of Medicine. Dr. West earned his Ph.D. in Immunobiology in 2011 and remained at Yale in the Department of Pathology for his postdoctoral fellowship. He joined MPIM in August 2016, and his lab is fully functional in the Immunology wing on the 4th floor of Reynolds. Current members of the lab include the Co-PI (Laura Ciaccia West), two postdoctoral associates (Christine Birdwell and Camila Guerra Martinez), a Ph.D. student (Abby Lei), and one undergraduate researcher (Melissa Pineda).
Q: WHAT DREW YOU TO TEXAS A&M?
A: I was attracted to the Department of Microbial Pathogenesis and Immunology at TAMHSC due to research strengths in innate immunity and host-pathogen interactions. I am particularly excited to expand my research into new infectious models to more broadly characterize how pathogens modulate mitochondrial function to enhance their virulence. I believe Texas A&M provides unique opportunities to achieve this goal via collaborations with investigators in my department and in other colleges across campus. Moreover, I am an innate immunologist by training, and the opportunity to join a department with a core group of researchers also focused on this area of immunobiology was appealing to me. Finally, my research program incorporates many animal models of human disease, and the strong Comparative Medicine program at TAMU, which oversees laboratory animal well-being and health, was very attractive.
Q: HOW DOES YOUR WORK FIT WITH THE RESEARCH ALREADY CONDUCTED HERE?
A: Many researchers on campus are investigating mitochondria in their specific systems, so my lab focus is related to ongoing work across the College of Medicine and beyond. There is increasing interest in these organelles, and since arriving at A&M, I have found it very easy to initiate collaborations with other labs pursuing aspects of mitochondrial research. For example, I am working with Ashok Shetty in the Department of Molecular and Cellular Medicine and the Institute for Regenerative Medicine to investigate how mitochondrial dysfunction contributes to the pathobiology of Gulf War Illness. We have recently been awarded a grant from the Department of Defense for this work and hope to begin the project this Fall.
Q: HOW DID YOU BECOME INTERESTED IN THIS RESEARCH?
A: My Ph.D. thesis with Sankar Ghosh focused on a novel adaptor protein in Toll-like receptor signaling named ECSIT. I started the project assuming the protein localized to the cytoplasm, similar to other intermediates in the pathway. In my fourth year of graduate study, I discovered that ECSIT localized to mitochondrial matrix. After much head scratching and a compete rewrite of my thesis aims, I sought out a collaborator at Yale, Gerry Shadel, to help me make sense of how a protein buried behind two mitochondrial membranes could connect to a cytosolic signaling pathway. Ultimately, my thesis lead me deep into the realm of mitochondrial biology, and I became so excited about the field that I stayed at Yale in Gerry Shadel’s lab for a postdoctoral fellowship. My postdoctoral research, which I am continuing here at A&M, largely focused on how mitochondria impact antiviral signaling and type I interferon responses in viral infections.
Q: YOUR RESEARCH LOOKS AT MANY WAYS MITROCHONDRIA AFFECT THE BODY, WHAT AREA ARE YOU MOST PASSIONATE ABOUT AND WHY?
A: My lab takes a ‘mitochondria-centric’ view of human health and disease. As critical participants in cellular energetics, signal transduction, and innate immunity, mitochondria are important organelles in nearly every cell in the body. Given these vital roles, mitochondrial dysfunction has been implicated in an ever-growing list of pathologies, including neurodegeneration, cancer, autoimmunity, and cardiovascular disease. A burgeoning area of mitochondrial research concerns how these organelles are centralized hubs in the innate immune system, and the bulk of our research is directed in this area. If we can understand how mitochondria guide immune responses in a variety of contexts, we may be able to shape these responses and influence inflammatory outcomes in many diseases.
Q: WHAT IS YOUR LONG-TERM GOAL FOR YOUR RESEARCH?
A: The overarching goal of my research is to better understand the mitochondrial etiology of disease and aging, which will hopefully lead to new avenues for therapeutic intervention to improve human health.