David Gonzalez, PhD
Assistant Professor, Department of Pharmacology
School of Medicine and the Skaggs School of Pharmacy
About the Awardee: Dr. Gonzalez received his B.A. at California State University, San Marcos. He received his Ph.D. in Biochemistry at the University of California, San Diego. His Ph.D. studies explored several creative avenues utilizing mass spectrometry to characterize the molecular output of bacteria from terrestrial and marine origins in new ways. He performed postdoctoral training supported by the A.P. Giannini Foundation for Medical Research in California, an NIH Institutional Research and Academic Career Development Award, and the prestigious UC President’s Fellowship at the University of California, San Diego. His current platform breaks the mold of traditional host-microbe research by utilizing innovative approaches in quantitative proteomics to rationalize further bench-top experimentation. Starting from a systems scale and narrowing to a single target approach, his lab is examining bacterial pathogenesis, host responses to infection, and the impact of the microbiome on health and disease. His contributions to innovative science, diversity, and mentoring were recognized in his induction into the Yale Edward A. Bouchet Graduate Honor Society, named in tribute to the first minority doctoral recipient in the United States.
Project Title: "Meta–omics Reveals Microbiome Driven Proteolysis as a Contributing Factor to Severity of Ulcerative Colitis Disease Activity"
Summary: Ulcerative colitis (UC) has a significant global burden, and is characterized by an aberrant immune response directed towards the gut microbiota. To better understand host-microbiome interactions governing UC, we collected and analyzed six fecal or serum based –omic datasets from 40 UC patients displaying a wide range of clinical, endoscopic, and histologic disease activity. Compounding evidence for proteolysis at higher disease severity was found, potentially mediated through the microbiome. Our in vitro and in vivo data suggest protease inhibition can be a viable avenue for UC treatment. Herein, we will further develop this work to study the proteases secreted by the gut microbiome that drive UC severity, and aim to identify the human targets of these proteases. To further inform this novel therapeutic approach, we will define the protease inhibitor class that may more effectively prevent microbiome-derived proteolysis with minimal side effects.