HMGB1 amplifies ILC2-induced type-2 inflammation and airway smooth muscle remodelling.
Loh, Z
Simpson, J
Ullah, A
Zhang, V
Gan, WJ
Lynch, JP
Werder, RB
Sikder, AA
Lane, K
Sim, CB
Porrello, E
Mazzone, SB
Sly, PD
Steptoe, RJ
Spann, KM
Sukkar, MB
Upham, JW
Phipps, S
- Publisher:
- Public Library of Science (PLoS)
- Publication Type:
- Journal Article
- Citation:
- PLoS pathogens, 2020, 16, (7)
- Issue Date:
- 2020-07-13
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Loh, Z | |
dc.contributor.author | Simpson, J | |
dc.contributor.author | Ullah, A | |
dc.contributor.author | Zhang, V | |
dc.contributor.author | Gan, WJ | |
dc.contributor.author | Lynch, JP | |
dc.contributor.author | Werder, RB | |
dc.contributor.author | Sikder, AA | |
dc.contributor.author | Lane, K | |
dc.contributor.author | Sim, CB | |
dc.contributor.author | Porrello, E | |
dc.contributor.author | Mazzone, SB | |
dc.contributor.author | Sly, PD | |
dc.contributor.author | Steptoe, RJ | |
dc.contributor.author | Spann, KM | |
dc.contributor.author | Sukkar, MB | |
dc.contributor.author | Upham, JW | |
dc.contributor.author | Phipps, S | |
dc.date.accessioned | 2020-09-25T05:18:34Z | |
dc.date.available | 2020-05-24 | |
dc.date.available | 2020-09-25T05:18:34Z | |
dc.date.issued | 2020-07-13 | |
dc.identifier.citation | PLoS pathogens, 2020, 16, (7) | |
dc.identifier.issn | 1553-7366 | |
dc.identifier.issn | 1553-7374 | |
dc.identifier.uri | http://hdl.handle.net/10453/142862 | |
dc.description.abstract | Type-2 immunity elicits tissue repair and homeostasis, however dysregulated type-2 responses cause aberrant tissue remodelling, as observed in asthma. Severe respiratory viral infections in infancy predispose to later asthma, however, the processes that mediate tissue damage-induced type-2 inflammation and the origins of airway remodelling remain ill-defined. Here, using a preclinical mouse model of viral bronchiolitis, we find that increased epithelial and mesenchymal high-mobility group box 1 (HMGB1) expression is associated with increased numbers of IL-13-producing type-2 innate lymphoid cell (ILC2s) and the expansion of the airway smooth muscle (ASM) layer. Anti-HMGB1 ablated lung ILC2 numbers and ASM growth in vivo, and inhibited ILC2-mediated ASM cell proliferation in a co-culture model. Furthermore, we identified that HMGB1/RAGE (receptor for advanced glycation endproducts) signalling mediates an ILC2-intrinsic IL-13 auto-amplification loop. In summary, therapeutic targeting of the HMGB1/RAGE signalling axis may act as a novel asthma preventative by dampening ILC2-mediated type-2 inflammation and associated ASM remodelling. | |
dc.format | Electronic-eCollection | |
dc.language | eng | |
dc.publisher | Public Library of Science (PLoS) | |
dc.relation.ispartof | PLoS pathogens | |
dc.relation.isbasedon | 10.1371/journal.ppat.1008651 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 0605 Microbiology, 1107 Immunology, 1108 Medical Microbiology | |
dc.subject.classification | Virology | |
dc.subject.mesh | Muscle, Smooth | |
dc.subject.mesh | Lymphocytes | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | HMGB1 Protein | |
dc.subject.mesh | Airway Remodeling | |
dc.subject.mesh | Receptor for Advanced Glycation End Products | |
dc.subject.mesh | Muscle, Smooth | |
dc.subject.mesh | Lymphocytes | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | HMGB1 Protein | |
dc.subject.mesh | Airway Remodeling | |
dc.subject.mesh | Receptor for Advanced Glycation End Products | |
dc.subject.mesh | Airway Remodeling | |
dc.subject.mesh | Animals | |
dc.subject.mesh | HMGB1 Protein | |
dc.subject.mesh | Inflammation | |
dc.subject.mesh | Lymphocytes | |
dc.subject.mesh | Mice | |
dc.subject.mesh | Muscle, Smooth | |
dc.subject.mesh | Receptor for Advanced Glycation End Products | |
dc.title | HMGB1 amplifies ILC2-induced type-2 inflammation and airway smooth muscle remodelling. | |
dc.type | Journal Article | |
utslib.citation.volume | 16 | |
utslib.location.activity | United States | |
utslib.for | 0605 Microbiology | |
utslib.for | 1107 Immunology | |
utslib.for | 1108 Medical Microbiology | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health/Graduate School of Health/GSH.Pharmacy | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Health/Graduate School of Health | |
utslib.copyright.status | open_access | * |
pubs.consider-herdc | false | |
dc.date.updated | 2020-09-25T05:18:30Z | |
pubs.issue | 7 | |
pubs.publication-status | Published | |
pubs.volume | 16 | |
utslib.citation.issue | 7 |
Abstract:
Type-2 immunity elicits tissue repair and homeostasis, however dysregulated type-2 responses cause aberrant tissue remodelling, as observed in asthma. Severe respiratory viral infections in infancy predispose to later asthma, however, the processes that mediate tissue damage-induced type-2 inflammation and the origins of airway remodelling remain ill-defined. Here, using a preclinical mouse model of viral bronchiolitis, we find that increased epithelial and mesenchymal high-mobility group box 1 (HMGB1) expression is associated with increased numbers of IL-13-producing type-2 innate lymphoid cell (ILC2s) and the expansion of the airway smooth muscle (ASM) layer. Anti-HMGB1 ablated lung ILC2 numbers and ASM growth in vivo, and inhibited ILC2-mediated ASM cell proliferation in a co-culture model. Furthermore, we identified that HMGB1/RAGE (receptor for advanced glycation endproducts) signalling mediates an ILC2-intrinsic IL-13 auto-amplification loop. In summary, therapeutic targeting of the HMGB1/RAGE signalling axis may act as a novel asthma preventative by dampening ILC2-mediated type-2 inflammation and associated ASM remodelling.
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