John Osterholzer, M.D.
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.
Research in my laboratory is focused on elucidating the role of lung dendritic cells (DC), monocytes, and macrophages in orchestrating adaptive immune responses in the lungs in response to infectious or inflammatory stimuli. We primarily utilize murine models of fungal infection (primarily Cryptococcus neoformans), to study mechanisms of DC recruitment, differentiation, activation, and their ability to influence T cell polarization within the lung microenvironment. In parallel, we also investigate the origin and functions of pulmonary monocytes and macrophage populations as cell types which also link innate and adaptive immune responses. We further explore molecular mechanisms of communication between the lung and bone marrow with a specific interest in the role of chemokine receptor 2 (CCR2) and GM-CSF in this process. Ongoing studies will continue to explore the mechanistic attributes of these cells (antigen presentation, fungicidal capacity) and investigate whether enhancing or diminishing the accumulation of these cells further alters the resultant immune response against the organism. In related work, we are also investigating the role of lung monocytes, DC, and macrophages in response to non-infectious lung epithelial cell injury and lung transplantation to determine whether (and how) these cells contribute to lung fibrosis.