The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders.

Chong, WC; Shastri, MD; Peterson, GM; Patel, RP; Pathinayake, PS; Dua, K; Hansbro, NG; Hsu, AC; Wark, PA; Shukla, SD; Johansen, MD; Schroder, K; Hansbro, PM

The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders.

Chong, WC Shastri, MD Peterson, GM Patel, RP Pathinayake, PS Dua, K

Hansbro, NG Hsu, AC Wark, PA Shukla, SD Johansen, MD Schroder, K Hansbro, PM

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Publisher:: Wiley
Publication Type:: Journal Article
Citation:: Clinical & translational immunology, 2021, 10, (2), pp. e1247
Issue Date:: 2021-01

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Field	Value	Language
dc.contributor.author	Chong, WC
dc.contributor.author	Shastri, MD
dc.contributor.author	Peterson, GM
dc.contributor.author	Patel, RP
dc.contributor.author	Pathinayake, PS
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159
dc.contributor.author	Hansbro, NG
dc.contributor.author	Hsu, AC
dc.contributor.author	Wark, PA
dc.contributor.author	Shukla, SD
dc.contributor.author	Johansen, MD
dc.contributor.author	Schroder, K
dc.contributor.author	Hansbro, PM
dc.date.accessioned	2021-03-18T22:26:23Z
dc.date.available	2021-01-10
dc.date.available	2021-03-18T22:26:23Z
dc.date.issued	2021-01
dc.identifier.citation	Clinical & translational immunology, 2021, 10, (2), pp. e1247
dc.identifier.issn	2050-0068
dc.identifier.issn	2050-0068
dc.identifier.uri	http://hdl.handle.net/10453/147353
dc.description.abstract	Inflammation is the result of a complex network of cellular and molecular interactions and mechanisms that facilitate immune protection against intrinsic and extrinsic stimuli, particularly pathogens, to maintain homeostasis and promote tissue healing. However, dysregulation in the immune system elicits excess/abnormal inflammation resulting in unintended tissue damage and causes major inflammatory diseases including asthma, chronic obstructive pulmonary disease, atherosclerosis, inflammatory bowel diseases, sarcoidosis and rheumatoid arthritis. It is now widely accepted that both endoplasmic reticulum (ER) stress and inflammasomes play critical roles in activating inflammatory signalling cascades. Notably, evidence is mounting for the involvement of ER stress in exacerbating inflammasome-induced inflammatory cascades, which may provide a new axis for therapeutic targeting in a range of inflammatory disorders. Here, we comprehensively review the roles, mechanisms and interactions of both ER stress and inflammasomes, as well as their interconnected relationships in inflammatory signalling cascades. We also discuss novel therapeutic strategies that are being developed to treat ER stress- and inflammasome-related inflammatory disorders.
dc.format	Electronic-eCollection
dc.language	eng
dc.publisher	Wiley
dc.relation	http://purl.org/au-research/grants/nhmrc/GNT1079187
dc.relation	http://purl.org/au-research/grants/nhmrc/1175134
dc.relation.ispartof	Clinical & translational immunology
dc.relation.isbasedon	10.1002/cti2.1247
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	1107 Immunology, 1115 Pharmacology and Pharmaceutical Sciences
dc.title	The complex interplay between endoplasmic reticulum stress and the NLRP3 inflammasome: a potential therapeutic target for inflammatory disorders.
dc.type	Journal Article
utslib.citation.volume	10
utslib.location.activity	Australia
utslib.for	1107 Immunology
utslib.for	1115 Pharmacology and Pharmaceutical Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Health
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/Faculty of Health/Graduate School of Health
pubs.organisational-group	/University of Technology Sydney/Faculty of Health/Graduate School of Health/GSH.Pharmacy
utslib.copyright.status	open_access	*
dc.date.updated	2021-03-18T22:26:19Z
pubs.issue	2
pubs.publication-status	Published
pubs.volume	10
utslib.citation.issue	2

Abstract:

Inflammation is the result of a complex network of cellular and molecular interactions and mechanisms that facilitate immune protection against intrinsic and extrinsic stimuli, particularly pathogens, to maintain homeostasis and promote tissue healing. However, dysregulation in the immune system elicits excess/abnormal inflammation resulting in unintended tissue damage and causes major inflammatory diseases including asthma, chronic obstructive pulmonary disease, atherosclerosis, inflammatory bowel diseases, sarcoidosis and rheumatoid arthritis. It is now widely accepted that both endoplasmic reticulum (ER) stress and inflammasomes play critical roles in activating inflammatory signalling cascades. Notably, evidence is mounting for the involvement of ER stress in exacerbating inflammasome-induced inflammatory cascades, which may provide a new axis for therapeutic targeting in a range of inflammatory disorders. Here, we comprehensively review the roles, mechanisms and interactions of both ER stress and inflammasomes, as well as their interconnected relationships in inflammatory signalling cascades. We also discuss novel therapeutic strategies that are being developed to treat ER stress- and inflammasome-related inflammatory disorders.

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http://hdl.handle.net/10453/147353