John F. Alcorn, PhD
- Professor of Pediatrics
- Associate Director, Richard King Mellon Foundation Institute for Pediatric Research
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
Education & Training
- BS, Biology/Pre-Medicine, Youngstown State University, 1996
- MS, Physiology, Youngstown State University, 1998
- PhD, Cell and Molecular Biology, Duke University Medical Center, 2003
- Postdoctoral Associate, University of Vermont Department of Pathology, 2004-2005
- Post-Doctoral Fellowship, University of Vermont Department of Pathology, 2005-2007
Alcorn JF, Avula R, Chakka AB, Schwarzmann WE, Nowalk MP, Lin CJ, Ortiz MA, Horne WT, Chandran UR, Nagg JP, Zimmerman RK, Cole KS, Moehling KK, Martin JM. Differential gene expression in peripheral blood mononuclear cells from children immunized with inactivated influenza vaccine. Hum Vaccin Immunother. 2020 Apr 16:1-9. Doi:10.1080/ 21645515.2020.1711677. [Epub ahead of print] PMID:32298194
van der Velden JL, Alcorn JF, Chapman DG, Lundblad LKA, Irvin CG, Davis RJ, Butnor K, Janssen-Heininger YMW. Airway epithelial specific deletion of Jun-N-terminal kinase 1 attenuates pulmonary fibrosis in two independent mouse models. PLoS One. 2020 Jan 14;15(1):e0226904. PMC6959564
Henkel M, Partyka J, Gregory AD, Forno E, Cho MH, Eddens T, Tout AR, Salamacha N, Horne W, Rao KS, Wu Y, Alcorn JF, Kostka D, Hirsch R, Celedón JC, Shapiro SD, Kolls JK, Campfield BT. Follistatin-like 1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema. Am J Respir Crit Care Med. 2019 Dec 13. doi: 10.1164/rccm.201905-0973OC. [Epub ahead of print] PMID:31834999
Sodhi CP, Nguyen J, Yamaguchi Y, Werts AD, Lu P, Ladd MR, Fulton WB, Kovler ML, Wang S, Prindle T Jr, Zhang Y, Lazartigues ED, Holtzman MJ, Alcorn JF, Hackam DJ, Jia H. A Dynamic Variation of Pulmonary ACE2 Is Required To Modulate Neutrophilic Inflammation in Response to Pseudomonas aeruginosa Lung Infection in Mice. J Immunol. 2019 Oct 23. pii: ji1900579. PMID:31645418
Trevejo-Nunez G, Elsegeiny W, Aggor FEY, Tweedle JL, Kaplan Z, Gandhi P, Castillo P, Ferguson A, Alcorn JF, Chen K, Kolls JK, Gaffen SL. Interleukin-22 (IL-22) Binding Protein Constrains IL-22 Activity, Host Defense, and Oxidative Phosphorylation Genes during Pneumococcal Pneumonia. Infect Immun. 2019 Oct 18;87(11). pii: e00550-19. PMC6803344
Hebert KD, Mclaughlin N, Zhang Z, Cipriani A, Alcorn JF, Pociask DA. IL-22Ra1 is induced during influenza infection by direct and indirect TLR3 induction of STAT1. Respir Res 20(1):184, 2019. PMC6694528
Robinson KM, Ramanan K, Tobin JM, Nickolich KL, Pilewski MJ, Kallewaard NL, Sellman BR, Cohen TS, and JF Alcorn. Survival during influenza-associated bacterial superinfection improves following viral- and bacterial-specific monoclonal antibody treatment. JCI Insight 4(14): pii: 125554, 2019. PMC6675563
Abood RN, McHugh KJ, Rich HE, Ortiz MA, Tobin JM, Ramanan K, Robinson KM, Bomberger JM, Kolls JK, Manni ML, Pociask DA, and JF Alcorn. IL-22-binding protein exacerbates influenza, bacterial super-infection. Mucosal Immunol 12(5):1231-1243, 2019. PMC6717528
Ackerman EE, Alcorn JF, Hase T, Shoemaker JE. A dual controllability analysis of influenza virus-host protein-protein interaction networks for antiviral drug target discovery. BMC Bioinformatics 20(1):297, 2019. PMC654573
Gopal R, Mendy A, Marinelli MA, Richwalls LJ, Seger PJ, Patel S, McHugh KJ, Rich HE, Grousd JA, Forno E, and JF Alcorn. Peroxisome Proliferator-Activated Receptor Gamma (PPARg) Suppresses Inflammation and Bacterial Clearance during Influenza-Bacterial Super-Infection. Viruses 11(6):pii: E505, 2019. PMC6630660
Academic and Research Interests
2R01HL107380-06, Influenza A Inhibits TH17 Host Defense Against Bacterial Pneumonia. (PI, 20% effort), 2017-2021, NIH NHLBI, $1,560,939 ($1,000,000 Direct Costs)
The role of IL-22 in Influenza, Staphylococcus aureus Super-Infection, (PI, 5% effort), 2017-2020, PA Department of Health, $284,000 (284,000 Direct Costs)
Vaccine Efficacy in Children, Option B, (PI, 10% effort), 2019-2020, CDC, $105,480 ($67,400 Direct Costs)
R33AI119258, Mucosally-derived HA stem binding antiviral for influenza. (PI, 10% effort), 2017-2020, NIH NIAID, $312,600 ($200,000 Direct Costs)
1R01HL126711, Combined Viral and Bacterial Infection and Zinc Homeostasis in Distal Lung, (PI, 5% effort) 2015-2021, NIH NHLBI, $31,861 (25,861 Direct Costs)
1R01HL141364, Unfolded Protein Response in Influenza Virus Infection and Inflammation, (PI, 10% effort), 2018-2023, NIH NHLBI, $505,920 ($325,000 Direct Costs)
1R01DK118033, Biomarkers for Urinary Tract Infection and Pyelonephritis, (PI, 5% effort), 2019-2023, NIH NIDDK, $155,902 ($99,618 Direct Costs)
Pittsburgh RDP CF Center Grant, Infection & Immunity Core, (PI, 15% effort), 2019-2023, Cystic Fibrosis Foundation, $313,200 ($200,000 Direct Costs)