Charles Dela Cruz, MD, PhD

Dr. Dela Cruz completed his research training through an MD/PhD program in the area of immunology and virology from University of Toronto and Yale. Clinically, he is trained in internal medicine, and specializes in pulmonary and critical care medicine and is currently an Associate Professor at Yale University in the same department. He is also the founding director for the Center for Pulmonary Infection Research and Treatment (CPIRT). www.cpirt.yale.edu. His laboratory is interested in studying the role of respiratory infection in the pathogenesis of acute and chronic lung diseases. Specifically, his work focuses on how lung infection contribute to inflammation, injury and tissue repair in the lung. This has allowed the lab to carefully study the molecular and cellular responses of several novel mediators in the lung.

His laboratory focuses on two main research programs. (1) Studying novel immune regulators in the lung during respiratory infections. (2) Studying the effects of cigarette smoke (CS) exposure in the pathogenesis of airway and lung diseases such as chronic obstructive pulmonary disease (COPD) using preclinical genetic mouse models and human biosamples. The goal of the lab is also to be able to confirm and translate the findings using biospecimens from the established and establishing cohort of human patients with various lung diseases.

COPD is a composite entity that includes chronic bronchitis and emphysema, is a leading cause of death in the world, and is a disease that is in need of new treatments. One of the goal of our laboratory is to investigate the interaction between CS and respiratory virus infection in the pathogenesis of COPD and identify novel therapeutic targets for this respiratory disease. It has been long thought that the frequent respiratory infections in COPD patients are due to their depressed immune function. Our studies have revealed that CS-exposed hosts have an over-exaggerated immune reaction to viral infections. Frequent acute COPD exacerbations correlate with increased rate of disease progression and more loss of lung function in COPD especially if it is due to viral infections. Our studies have shown that CS exposure has an impressive ability to regulate the innate immunity in the lung after influenza virus and respiratory syncytial virus (RSV) infection. CS enhances the inflammation, alveolar destruction and airway fibrosis caused by influenza virus and RSV. These effects are mediated by type I interferon and RIG-like helicase antiviral innate immune pathway. CS exposure also results in the induction of interleukin-15 in the setting of these respiratory infections. We hypothesize that these novel mechanistic pathways may explain the heightened inflammatory response and worsening lung functions in COPD patients with multiple virally-induced exacerbations, and the chronic lung inflammation seen in stable COPD patients. We have also translated our findings by studying these immune mediators in patients infected with various respiratory viruses and have thus far collected >300 human biosamples.
YCCI Scholar 2011