Dr. Curtis received his medical degree from the Georgetown University School of Medicine. After a clinical residency in internal medicine and a year as Chief Medical Resident at the Johns Hopkins Bayview Medical Center, he spent two years as a Clinical Immunology Fellow at the National Institute on Aging, NIH. He then trained in Pulmonary & Critical Care Medicine (PCCM) at the University of California San Francisco, where he joined the faculty at the San Francisco VA. Dr. Curtis was previously Chief, PCCM Section at the VA Ann Arbor Healthcare System (19990-2014) where he was scientific director of a Research Enhancement Award Program center in tobacco-induced lung diseases (1999-2012). He has held leadership roles in multiple COPD clinical trials, including the ongoing SPIROMICS and COPDGene® studies. He is an Associate Editor of the American Journal of Respiratory & Critical Care Medicine and past-Chair of the American Thoracic Scientific Assembly on Allergy, Immunology & Inflammation, from which he received a lifetime scientific achievement award in 2019. Dr. Curtis is an avid cyclist and downhill skier who enjoys cooking and eating many international cuisines, and reading, especially world history.
Lung immunity in humans and mice.
Specifically: immunopathogenesis of COPD; Efferocytosis; Interactions of lung leukocytes with the lung microbiome.
The Curtis lab studies the regulation of pulmonary immunity by lung leukocytes. As a practicing physician involved in multiple clinical studies, the PI has direct access to unique human samples and clinical data. While we use a wide variety of experimental techniques, our forte is advanced flow cytometry, made possible by our own modified LSR II flow cytometer. We also collaborate with a number of other PIBS labs, especially on murine projects and for analysis of the lung microbiome. We welcome graduate students interested in rotations.
Active projects include:
Immunopathogenesis of chronic obstructive pulmonary disease (COPD), through analysis of leukocytes from human lung tissue, bronchoalveolar lavage and peripheral blood. COPD is a complex group of lung disorders resulting from oxidative damage by smoking or, especially in the developing world, from indoor air pollution. It is currently the third-leading cause of death in the USA, and is projected by the World Health Organization (WHO) to be THE leading cause of death worldwide by 2050. Immune mechanisms appear to be central, but are only beginning to be defined.
Molecular mechanisms and consequences of apoptotic cell ingestion by murine & human alveolar macrophages. In healthy individuals, billions of cells die by apoptosis each day. Clearance of these apoptotic cells, termed “efferocytosis,” must be efficient to prevent secondary necrosis and the release of proinflammatory cell contents that disrupt homeostasis and potentially foster autoimmunity. During inflammation, most apoptotic cells are cleared by macrophages; the efferocytic process actively induces a macrophage phenotype that favors tissue repair and suppression of inflammation. Chronic lung diseases such as COPD, asthma, and cystic fibrosis are characterized by an increased lung burden of uningested apoptotic cells.
Interactions of lung leukocytes with the lung microbiome. The lower respiratory tracts are not sterile in healthy individuals as previously believed, but instead appear to harbor very small numbers (relative to other bodily surfaces) of bacteria, viruses and fungi. In collaboration with other UM labs, all members of the Lung HIV Microbiome Project, we seek to define the interactions between host immunity and microbes, and among the various microbes themselves, that maintain health or contribute to disease progression.