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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
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Complement-mediated 'bystander' damage initiates host NLRP3 inflammasome activation.
Rahul Suresh1, Prabha Chandrasekaran1, Fayyaz S Sutterwala2
1Department of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD 20742, USA.
Journal of Cell Science
|March 24, 2016
Summary
Phagocytosis of complement-opsonized particles triggers inflammation via the membrane attack complex (MAC) transferring to macrophages. This activates the NLRP3 inflammasome, leading to cytokine release and immune cell modulation.
Area of Science:
- Immunology
- Cell Biology
- Inflammation Research
Background:
- Complement activation traditionally linked to inflammation via C3a and C5a.
- A novel mechanism involving terminal complement components is investigated.
Purpose of the Study:
- To elucidate a new pathway for complement-mediated inflammation during phagocytosis.
- To determine the role of the membrane attack complex (MAC) in inflammasome activation.
Main Methods:
- Phagocytosis assays using complement-opsonized and unopsonized particles.
- Analysis of inflammasome activation (NLRP3, caspase-1) and cytokine secretion (IL-1β, IL-18).
- Assessment of immune cell recruitment and T helper 17 cell polarization.
Main Results:
- Membrane attack complex (MAC) transfer from particles to macrophages initiates NLRP3 inflammasome activation.
- IL-1β and IL-18 secretion is dependent on NLRP3, ASC, and caspase-1.
- Complement-opsonized particle phagocytosis enhances leukocyte recruitment and TH17 cell biasing.
Conclusions:
- A novel MAC-dependent mechanism drives complement-mediated inflammation.
- This pathway regulates both innate and adaptive immune responses.
- Findings reveal new therapeutic targets for inflammatory diseases.
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