Airway epithelial cells (AEC) exhibit a pro-inflammatory phenotype in patients with allergic asthma. We examined the effect of an allergic cytokine environment on the response of AEC to rhinovirus (RV), the most common trigger of acute exacerbations of asthma. Calu-3 cells, a well-differentiated human AEC line, were cultured with or without the T-helper type 2 cytokines interleukin (IL)-4 and IL-13, then stimulated with a toll-like receptor (TLR) 3 agonist (poly I:C, dsRNA) or a TLR7 agonist (imiquimod), or infected with RV 16. Expression of pro-inflammatory and antiviral mediators, and of viral pattern-recognition molecules, was assessed using nCounter assays, quantitative real-time PCR (qRT-PCR) and protein immunoassays. Both dsRNA and imiquimod stimulated expression of mRNA for IL6 and IL8 whereas expression of several chemokines and antiviral response genes was induced only by dsRNA. Conversely, expression of other cytokines and growth factors was induced only by imiquimod. RV infection not only stimulated expression of the inflammation-related genes induced by dsRNA, but also of complement factor B and the novel pro-inflammatory cytokine IL-32. In the T helper type 2 (Th2) cytokine environment, several mediators exhibited significantly enhanced expression, whereas expression of interferons was either unchanged or enhanced. The allergic environment also increased expression of pattern-recognition receptors and of intercellular adhesion molecule 1, the cell surface receptor for RV. We conclude that Th2 cytokines promote increased production of pro-inflammatory mediators by AEC following infection with RV. Increased viral entry or enhanced signalling via pattern-recognition receptors could also contribute to the exaggerated inflammatory response to RV observed in allergic asthmatics.
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Phase contrast microscopy showing primary human mesangial cells in culture. Quantification of cell area showed that exposure of mesangial cells to the pro-fibrotic growth factor (TGF-β1) induced morphological cell expansion and hypertrophy, which was reversed following the overexpression of miR-378. Interestingly, transfection of a miR-378 inhibitor induced the expansion of mesangial cells, highlighting the regulatory role of miR-378 in mesangial hypertrophy. Please see the article by Wang et al. (pages 411-423).
Research Article|
March 06 2017
Allergic environment enhances airway epithelial pro-inflammatory responses to rhinovirus infection
Cristan Herbert;
Cristan Herbert
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
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Kimchi Do;
Kimchi Do
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
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Vincent Chiu;
Vincent Chiu
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
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Linda Garthwaite;
Linda Garthwaite
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
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Yifan Chen;
Yifan Chen
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
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Paul M. Young;
Paul M. Young
2Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2037, Australia
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Daniela Traini;
Daniela Traini
2Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW 2037, Australia
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Rakesh K. Kumar
1Department of Pathology, School of Medical Sciences, UNSW Sydney, NSW 2052, Australia
Correspondence: Rakesh K. Kumar ([email protected])
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Publisher: Portland Press Ltd
Received:
December 06 2016
Revision Received:
January 19 2017
Accepted:
January 21 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (6): 499–509.
Article history
Received:
December 06 2016
Revision Received:
January 19 2017
Accepted:
January 21 2017
Citation
Cristan Herbert, Kimchi Do, Vincent Chiu, Linda Garthwaite, Yifan Chen, Paul M. Young, Daniela Traini, Rakesh K. Kumar; Allergic environment enhances airway epithelial pro-inflammatory responses to rhinovirus infection. Clin Sci (Lond) 1 March 2017; 131 (6): 499–509. doi: https://doi.org/10.1042/CS20160939
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