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Zinc depletion regulates the processing and secretion of IL-1β

H Summersgill, H England, G Lopez-Castejon, C B Lawrence, N M Luheshi, J Pahle, P Mendes, D Brough

Cell Death & Disease. 2014;5.

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Abstract

Sterile inflammation contributes to many common and serious human diseases. The pro-inflammatory cytokine interleukin-1β (IL-1β) drives sterile inflammatory responses and is thus a very attractive therapeutic target. Activation of IL-1β in sterile diseases commonly requires an intracellular multi-protein complex called the NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome. A number of disease-associated danger molecules are known to activate the NLRP3 inflammasome. We show here that depletion of zinc from macrophages, a paradigm for zinc deficiency, also activates the NLRP3 inflammasome and induces IL-1β secretion. Our data suggest that zinc depletion damages the integrity of lysosomes and that this event is important for NLRP3 activation. These data provide new mechanistic insight to how zinc deficiency contributes to inflammation and further unravel the mechanisms of NLRP3 inflammasome activation.

Bibliographic metadata

Type of resource:
Content type:
Publication status:
Published
Publication type:
Publication form:
Published date:
Accepted date:
2013-12-09
Submitted date:
2013-08-29
Language:
eng
Journal title:
Abbreviated journal title:
ISSN:
Publishers website:
http://www.nature.com/cddis/journal/v5/n1/full/cddis2013547a.html
Volume:
5
Article number:
e1040
Digital Object Identifier:
10.1038/cddis.2013.547
Attached files Open Access licence:
Creative Commons Attribution (CC BY)
Attached files embargo period:
Immediate release
Attached files release date:
19th June, 2014
Access state:
Active

Institutional metadata

University researcher(s):

Record metadata

Manchester eScholar ID:
uk-ac-man-scw:227430
Created by:
Pedrosa Mendes, Pedro
Created:
19th June, 2014, 15:21:23
Last modified by:
Pedrosa Mendes, Pedro
Last modified:
19th June, 2014, 15:21:23

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