Dr. Koon is an associate professor in UCLA’s Vatche and Tamar Manoukian Division of Digestive Diseases. He received a master’s degree in pharmacology and a PhD in molecular biology from the University of Hong Kong. He then completed his postdoctoral training in gastroenterology at the Beth Israel Deaconess Medical Center of Harvard Medical School in Boston.
Dr. Koon focuses on basic, clinical, and translational research on inflammatory bowel disease (IBD), C. difficile infection, and metabolic diseases. Over the last decade, Dr. Koon has been successful in discovering antimicrobial peptides cathelicidin as a serum biomarker for indicating the presence of intestinal strictures in Crohn’s disease (CD) patients and predicting the future clinical activity in IBD patients. Some of his inventions were patented and licensed to a diagnostic company for commercial development.
In recent years, Dr. Koon has established a biobank that consists of blood, serum exosomes, mesenteric and skin adipose tissues, and intestinal tissues from healthy subjects and IBD patients. By utilizing next-generation transcriptome analysis, he identified multiple biomarkers and molecular targets that might be relevant to intestinal fibrosis. Dr. Koon developed a convenient machine-learning algorithm for an accurate indication of the presence of intestinal strictures in CD patients and discovered the chemical communication between fat and intestine during intestinal fibrosis development.
Dr. Koon is actively involved in developing new therapeutic approaches for gastrointestinal diseases. He utilized an orally active modified cathelicidin mimic CSA13-Eudragit formulation for reversing colitis-associated intestinal fibrosis and C. difficile infection (CDI). His discoveries were published in Scientific Reports and Gastroenterology. Oral administration of CSA13-Eudragit ameliorates intestinal inflammation via modulation of the intestinal microbiome environment. Through untargeted metabolomics studies, he identified several orally active therapeutic metabolites, which are effective against intestinal fibrosis and CDI.
In recent years, Dr. Koon has been collaborating with multiple pharmaceutical companies in drug development. He utilized whole-transcriptome RNA sequencing and multiplex assays to discover molecular targets in C. difficile infection (CDI). For example, he identified macrophage inflammatory protein-1 alpha (MIP-1?) as a common CDI mediator among humans and mice. MIP-1? specifically mediates inflammatory responses and diarrhea during CDI. Therefore, this immunological discovery is useful for evaluating disease activity in CDI as well as therapy development against CDI.
Dr. Koon was the first to discover the role of antimicrobial peptides (cathelicidin and elafin) in obesity and prediabetes, and type II diabetes. He observed abnormal levels of serum cathelicidin and elafin in patients with prediabetes and type II diabetes. Cathelicidin regulates obesity and non-alcoholic fatty liver disease (NAFLD) in high-fat diet-treated mice via the reduction of CD36 expression. Recently, Dr. Koon generated an orally active modified elafin formulation for influencing miRNA load in serum exosomes. The serum exosomes carry miRNAs that improve leptin sensitivity and increase leptin expression, leading to reduced food intake. As a result, the food intake suppression subsequently ameliorates obesity, hyperglycemia, and liver steatosis in high-fat diet-treated mice.
Dr. Koon has published 43 peer-reviewed manuscripts. Dr. Koon’s projects have been funded by CCF, NIH, Broad Foundation, and industrial funding. His research team consists of a postdoctoral researcher, a medical resident, a technician, and several undergraduate research students. His laboratory, at the MacDonald Research Laboratories building, is a hub of researcher interactions. His team works to develop advanced research platforms such as 3D organoid and ex-vivo cultures, high-throughput screening, and manipulation of microbiota and immune system. Dr. Koon’s research provides an integrated view of interactions between different systems. He welcomes research collaborations for discovering solutions for gastrointestinal and metabolic diseases.
