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Article

Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model

1
Commonwealth Scientific and Industrial Research Organisation (CSIRO) Health and Biosecurity Business Unit, Australian Centre for Disease Preparedness (ACDP), Geelong, VIC 3220, Australia
2
CSIRO Australian Animal Health Laboratory (AAHL) Business Unit, ACDP, Geelong, VIC 3220, Australia
3
School of Medicine, Deakin University, Waurn Ponds, VIC 3216, Australia
*
Author to whom correspondence should be addressed.
Viruses 2020, 12(6), 679; https://doi.org/10.3390/v12060679
Received: 20 May 2020 / Revised: 19 June 2020 / Accepted: 22 June 2020 / Published: 24 June 2020
(This article belongs to the Section Animal Viruses)
The respiratory Influenza A Viruses (IAVs) and emerging zoonotic viruses such as Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) pose a significant threat to human health. To accelerate our understanding of the host–pathogen response to respiratory viruses, the use of more complex in vitro systems such as normal human bronchial epithelial (NHBE) cell culture models has gained prominence as an alternative to animal models. NHBE cells were differentiated under air-liquid interface (ALI) conditions to form an in vitro pseudostratified epithelium. The responses of well-differentiated (wd) NHBE cells were examined following infection with the 2009 pandemic Influenza A/H1N1pdm09 strain or following challenge with the dsRNA mimic, poly(I:C). At 30 h postinfection with H1N1pdm09, the integrity of the airway epithelium was severely impaired and apical junction complex damage was exhibited by the disassembly of zona occludens-1 (ZO-1) from the cell cytoskeleton. wdNHBE cells produced an innate immune response to IAV-infection with increased transcription of pro- and anti-inflammatory cytokines and chemokines and the antiviral viperin but reduced expression of the mucin-encoding MUC5B, which may impair mucociliary clearance. Poly(I:C) produced similar responses to IAV, with the exception of MUC5B expression which was more than 3-fold higher than for control cells. This study demonstrates that wdNHBE cells are an appropriate ex-vivo model system to investigate the pathogenesis of respiratory viruses. View Full-Text
Keywords: epithelium; lung; innate immune system; cytokine; chemokine; antiviral; tight junction; cell death; cytoskeleton; inflammation epithelium; lung; innate immune system; cytokine; chemokine; antiviral; tight junction; cell death; cytoskeleton; inflammation
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MDPI and ACS Style

Pharo, E.A.; Williams, S.M.; Boyd, V.; Sundaramoorthy, V.; Durr, P.A.; Baker, M.L. Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model. Viruses 2020, 12, 679. https://doi.org/10.3390/v12060679

AMA Style

Pharo EA, Williams SM, Boyd V, Sundaramoorthy V, Durr PA, Baker ML. Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model. Viruses. 2020; 12(6):679. https://doi.org/10.3390/v12060679

Chicago/Turabian Style

Pharo, Elizabeth A., Sinéad M. Williams, Victoria Boyd, Vinod Sundaramoorthy, Peter A. Durr, and Michelle L. Baker. 2020. "Host–Pathogen Responses to Pandemic Influenza H1N1pdm09 in a Human Respiratory Airway Model" Viruses 12, no. 6: 679. https://doi.org/10.3390/v12060679

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