John alcon

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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 under the mentorship of Dr. Jay Kolls. Alcorn is a recipient of the Parker B. 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.

Differential gene expression in peripheral blood mononuclear cells from children immunized with inactivated influenza vaccine. Hum Vaccin Immunother. Airway epithelial specific deletion of Jun-N-terminal kinase 1 attenuates pulmonary fibrosis in two independent mouse models. PLoS One. J Immunol. Infect Immun. 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. Differential gene expression in peripheral blood mononuclear cells from children immunized with inactivated influenza vaccine. Hum Vaccin Immunother. Airway epithelial specific deletion of Jun-N-terminal kinase 1 attenuates pulmonary fibrosis in two independent mouse models.

PLoS One. J Immunol. Infect Immun. Respir Res 20 1 , Survival during influenza-associated bacterial superinfection improves following viral- and bacterial-specific monoclonal antibody treatment.

JCI Insight 4 14 : pii: , ILbinding protein exacerbates influenza, bacterial super-infection. Mucosal Immunol 12 5 , A dual controllability analysis of influenza virus-host protein-protein interaction networks for antiviral drug target discovery.

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