Departments & Organizations
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 Assistant Professor at Yale University in the same department. His laboratory is interested in studying the pathogenesis of inflammation, injury and repair in the lung using genetically modified animals. This has allowed the lab to carefully study the molecular and cellular responses of certain novel mediators in the lung. His laboratory focuses on two main research programs. (1) 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. (2) Studying novel immune regulators in the lung during respiratory infections. 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 >200 human biosamples.
YCCI Scholar 2011
Project:07/01/11 - 06/30/13
Cigarette Smoke Exposure & Respiratory Virus Infection Interplay in Human Lung Diseases
Education & Training
|MD||Yale University School of Medicine (2003)|
|PhD||University of Toronto (2000)|
|BS||University of Toronto (1994)|
|Fellow||Yale University School of Medicine|
|Resident||Yale University School of Medicine|
|Board Certification||AB of Internal Medicine, Pulmonary Disease (2008)|
|Board Certification||AB of Internal Medicine, Critical Care Medicine (Internal Medicine) (2010)|