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Updated: Jun 19, 2026
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
CARD9 negatively regulates NLRP3-induced IL-1β production on Salmonella infection of macrophages
Milton Pereira1, Panagiotis Tourlomousis1, John Wright1
1Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES, UK.
Insights
Caspase recruitment domain-containing protein 9 (CARD9) negatively regulates Interleukin-1β (IL-1β) production during bacterial infections. CARD9 suppression during Salmonella infection enhances IL-1β, highlighting its role in pathogen-specific inflammatory responses.
Area of Science:
- Immunology
- Molecular Biology
- Microbiology
Background:
- Interleukin-1β (IL-1β) is a crucial proinflammatory cytokine for controlling bacterial infections.
- Tight regulation of IL-1β production is essential to prevent excessive inflammation.
Purpose of the Study:
- To investigate the role of caspase recruitment domain-containing protein 9 (CARD9) in IL-1β production during bacterial infection.
- To elucidate the mechanism by which CARD9 modulates the inflammatory response to Salmonella.
Main Methods:
- Investigated CARD9's function in IL-1β regulation during Salmonella infection.
- Analyzed CARD9's impact on pro-IL-1β expression, NLRP3 activation, and caspase-8 activity.
- Examined CARD9 expression levels during Salmonella enterica serovar Typhimurium infection.
Main Results:
- CARD9 negatively regulates IL-1β production by fine-tuning pro-IL-1β expression.
- CARD9 modulates spleen tyrosine kinase (SYK)-mediated NLRP3 inflammasome activation.
- CARD9 represses inflammasome-associated caspase-8 activity.
- CARD9 expression is suppressed during Salmonella Typhimurium infection, leading to increased IL-1β production.
Conclusions:
- CARD9 acts as a negative regulator of IL-1β during bacterial infections, particularly Salmonella.
- CARD9 functions as a central signaling hub coordinating pathogen-specific inflammatory responses.
- Understanding CARD9's role is critical for managing inflammatory responses in bacterial infections.
Abstract:
Interleukin-1β (IL-1β) is a proinflammatory cytokine required for host control of bacterial infections, and its production must be tightly regulated to prevent excessive inflammation. Here we show that caspase recruitment domain-containing protein 9 (CARD9), a protein associated with induction of proinflammatory cytokines by fungi, has a negative role on IL-1β production during bacterial infection. Specifically, in response to activation of the nucleotide oligomerization domain receptor pyrin-domain containing protein 3 (NLRP3) by Salmonella infection, CARD9 negatively regulates IL-1β by fine-tuning pro-IL-1β expression, spleen tyrosine kinase (SYK)-mediated NLRP3 activation and repressing inflammasome-associated caspase-8 activity. CARD9 is suppressed during Salmonella enterica serovar Typhimurium infection, facilitating increased IL-1β production. CARD9 is, therefore, a central signalling hub that coordinates a pathogen-specific host inflammatory response.
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