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Cutting edge: The NLRP3 inflammasome links complement-mediated inflammation and IL-1β release

Laudisi, F., Spreafico, R., Evrard, M., Hughes, Timothy Richard ORCID:, Mandriani, B., Kandasamy, M., Morgan, Bryan Paul ORCID:, Sivasankar, B. and Mortellaro, A. 2013. Cutting edge: The NLRP3 inflammasome links complement-mediated inflammation and IL-1β release. The Journal of Immunology 191 (3) , pp. 1006-1010. 10.4049/jimmunol.1300489

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The complement system is a potent component of the innate immune response, promoting inflammation and orchestrating defense against pathogens. However, dysregulation of complement is critical to several autoimmune and inflammatory syndromes. Elevated expression of the proinflammatory cytokine IL-1β is often linked to such diseases. In this study, we reveal the mechanistic link between complement and IL-1β secretion using murine dendritic cells. IL-1β secretion occurs following intracellular caspase-1 activation by inflammasomes. We show that complement elicits secretion of both IL-1β and IL-18 in vitro and in vivo via the NLRP3 inflammasome. This effect depends on the inflammasome components NLRP3 and ASC, as well as caspase-1 activity. Interestingly, sublethal complement membrane attack complex formation, but not the anaphylatoxins C3a and C5a, activated the NLRP3 inflammasome in vivo. These findings provide insight into the molecular processes underlying complement-mediated inflammation and highlight the possibility of targeting IL-1β to control complement-induced disease and pathological inflammation.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Subjects: Q Science > QR Microbiology > QR180 Immunology
R Medicine > R Medicine (General)
R Medicine > RM Therapeutics. Pharmacology
Publisher: American Association of Immunologists
ISSN: 0022-1767
Date of First Compliant Deposit: 30 March 2016
Last Modified: 25 Oct 2022 10:14

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