John F. Alcorn, PhD

Alcorn has held a long-standing interest in mucosal immunology. The interface between the host and the environment is exceptionally intriguing. The lung provides an outstanding model of these interactions where critical physiologic function meets host defense.

Alcorn received his PhD in Cell and Molecular Biology from Duke University in 2003. During this time he worked with Dr. Jo Rae Wright on the host defense properties of lung surfactant proteins in the context of bacterial pneumonia and cystic fibrosis. Following this training, he completed a post-doctoral fellowship at the University of Vermont Lung Center with Dr. Yvonne Janssen-Heininger. His projects were focused on inflammatory signaling in mouse models of asthma and chronic lung injury.

Throughout his training he gained expertise in immunology, cell biology, molecular biology, lung physiology, and disease modeling. Alcorn then joined the Department of Pediatrics as junior faculty in 2007 under the mentorship of Dr. Jay Kolls.  Alcorn is a recipient of the Parker B. Francis Foundation Jo Rae Wright Award for Scientific Excellence for his contributions to pulmonary disease research, a member of the steering committee for the University of Pittsburgh Cystic Fibrosis Center, an executive committee member of the ATS Allergy, Immunology, and Inflammation Assembly, and a standing member of the NIH Immunity and Host Defense Study Section.

The Alcorn laboratory is focused on pulmonary immunity, host defense, epithelial cell biology, and lung physiology as it relates to pediatric disease. A primary laboratory focus is on influenza infection and host defense mechanisms in the lung. Influenza presents a global health challenge for which there are limited therapeutics options. The laboratory is interested in understanding key factors involved in influenza pathogenesis and host mediated immunopathology. Recent studies in the lab are focused on how preceding influenza infection suppresses the ability of the lung to respond to secondary bacterial infections. We have shown that influenza inhibits Type 17 immune activation upon secondary challenge with MRSA resulting in attenuated clearance. These data identified a novel immune mechanism involved in increased susceptibility following viral infection. Over the last 10 years, the laboratory has extended its focus to fully elucidate immune dysfunction during influenza and influenza, bacterial super-infection.

The Alcorn laboratory is also working on human immune responses to influenza vaccination and infection. These studies conducted in partnership with the CDC are focused on cell mediated immunity. The current laboratory focus combines mouse models of human lung disease with translational studies utilizing the significant access to samples here at UPMC Children’s Hospital of Pittsburgh. The group’s goal is to model human disease, as best as possible, and elucidate novel mechanisms of disease pathogenesis in order to inform therapeutic design.

Professional and Scientific Society Memberships

• American Thoracic Society, 2005-Present
• American Association of Immunologists, 2013-Present
• Society for Pediatric Research, 2016-Present