Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma

Hansbro, PM; Kim, RY; Starkey, MR; Donovan, C; Dua, K; Mayall, JR; Liu, G; Hansbro, NG; Simpson, JL; Wood, LG; Hirota, JA; Knight, DA; Foster, PS; Horvat, JC

Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma

Hansbro, PM

Kim, RY

Starkey, MR Donovan, C Dua, K

Mayall, JR Liu, G

Hansbro, NG Simpson, JL Wood, LG Hirota, JA Knight, DA Foster, PS Horvat, JC

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Publication Type:: Journal Article
Citation:: Immunological Reviews, 2017, 278 (1), pp. 41 - 62
Issue Date:: 2017-07-01

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Field	Value	Language
dc.contributor.author	Hansbro, PM https://orcid.org/0000-0002-4741-3035	en_US
dc.contributor.author	Kim, RY https://orcid.org/0000-0002-8709-5270	en_US
dc.contributor.author	Starkey, MR	en_US
dc.contributor.author	Donovan, C	en_US
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159	en_US
dc.contributor.author	Mayall, JR	en_US
dc.contributor.author	Liu, G https://orcid.org/0000-0002-0489-2638	en_US
dc.contributor.author	Hansbro, NG	en_US
dc.contributor.author	Simpson, JL	en_US
dc.contributor.author	Wood, LG	en_US
dc.contributor.author	Hirota, JA	en_US
dc.contributor.author	Knight, DA	en_US
dc.contributor.author	Foster, PS	en_US
dc.contributor.author	Horvat, JC	en_US
dc.date.issued	2017-07-01	en_US
dc.identifier.citation	Immunological Reviews, 2017, 278 (1), pp. 41 - 62	en_US
dc.identifier.issn	0105-2896	en_US
dc.identifier.uri	http://hdl.handle.net/10453/125115
dc.description.abstract	© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.	en_US
dc.relation.ispartof	Immunological Reviews	en_US
dc.relation.isbasedon	10.1111/imr.12543	en_US
dc.subject.classification	Immunology	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Asthma	en_US
dc.subject.mesh	Respiratory Hypersensitivity	en_US
dc.subject.mesh	Obesity	en_US
dc.subject.mesh	Disease Models, Animal	en_US
dc.subject.mesh	Steroids	en_US
dc.subject.mesh	Anti-Asthmatic Agents	en_US
dc.subject.mesh	Treatment Outcome	en_US
dc.subject.mesh	Severity of Illness Index	en_US
dc.subject.mesh	Risk Factors	en_US
dc.subject.mesh	Air Pollution	en_US
dc.subject.mesh	Signal Transduction	en_US
dc.subject.mesh	Gene Expression Regulation	en_US
dc.subject.mesh	Drug Resistance	en_US
dc.subject.mesh	Diet, High-Fat	en_US
dc.title	Mechanisms and treatments for severe, steroid-resistant allergic airway disease and asthma	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.citation.volume	278	en_US
utslib.for	1107 Immunology	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Graduate School of Health
utslib.copyright.status	closed_access
pubs.issue	1	en_US
pubs.publication-status	Published	en_US
pubs.volume	278	en_US

Abstract:

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Severe, steroid-resistant asthma is clinically and economically important since affected individuals do not respond to mainstay corticosteroid treatments for asthma. Patients with this disease experience more frequent exacerbations of asthma, are more likely to be hospitalized, and have a poorer quality of life. Effective therapies are urgently required, however, their development has been hampered by a lack of understanding of the pathological processes that underpin disease. A major obstacle to understanding the processes that drive severe, steroid-resistant asthma is that the several endotypes of the disease have been described that are characterized by different inflammatory and immunological phenotypes. This heterogeneity makes pinpointing processes that drive disease difficult in humans. Clinical studies strongly associate specific respiratory infections with severe, steroid-resistant asthma. In this review, we discuss key findings from our studies where we describe the development of representative experimental models to improve our understanding of the links between infection and severe, steroid-resistant forms of this disease. We also discuss their use in elucidating the mechanisms, and their potential for developing effective therapeutic strategies, for severe, steroid-resistant asthma. Finally, we highlight how the immune mechanisms and therapeutic targets we have identified may be applicable to obesity-or pollution-associated asthma.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/125115