John Osterholzer, M.D.

Associate Professor of Internal Medicine, Pulmonary and Critical Care Division
Veteran Affairs Ann Arbor Healthcare System


I was granted my undergraduate degree at the University of Michigan (B.S.; Biology) in 1994 having also completed an Undergraduate Honors Thesis in the field of Tumor Immunotherapy (Mentor Bernard Fox, Ph.D.). I obtained my Medical Degree from the University of Michigan Medical School in 1999 having also completed additional graduate school classes and research rotations through the Department of Pathology (Mentor James Mule, Ph.D.). I completed Residency Training in Internal Medicine at the University of Michigan Health System from 1999-2002. From 2002-2003 I completed a postdoctoral fellowship in Pulmonary Immunology funded by the Department of Veterans Affairs Research Enhancement Program (Mentor Jeffrey Curtis, M.D.). Thereafter, I completed a Pulmonary and Critical Care Fellowship Training Program (2003-2006) with additional primary research training in the field of Pulmonary Immunology (Mentor Galen Toews, M.D.). Since 2006 I have been a Faculty Member in the Division of Pulmonary and Critical Care Medicine at the University of Michigan Health System and the Ann Arbor VA Health System. I was appointed Assistant Professor in the Department of Internal Medicine and a Faculty Member in the Graduate Program in Immunology in 2010. I’ve since been promoted to Associate Professor in 2016 and in 2019 I was named as the VA Ann Arbor Site Leader for the VA Post-Deployment Cardiopulmonary Evaluation Network.

Research Interests

Our laboratory remains exceedingly interested in understanding how resident and recruited populations of lung myeloid cells, especially macrophages, monocytes, and dendritic cells, both initiate and orchestrate immune responses in the lung. We have characterized the contribution of these cells in response to cryptococcal lung infection and have more recently shifted our focus to better understand their role in responding to epithelial cell injury and the manner in which they contribute to the development of lung fibrosis.