Related Experiment Video

Updated: Apr 20, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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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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Toll-like receptor 2 and NLRP3 cooperate to recognize a functional bacterial amyloid, curli

Glenn J Rapsinski1, Meghan A Wynosky-Dolfi2, Gertrude O Oppong1

  • 1Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, Pennsylvania, USA.

Infection and Immunity
|November 26, 2014
PubMed

Insights

Bacterial amyloids, like curli fibers, activate the NLRP3 inflammasome, triggering interleukin-1β (IL-1β) production. This process involves Toll-like receptor 2 (TLR2) and does not induce cell death in macrophages.

Area of Science:

  • Immunology
  • Microbiology
  • Biochemistry

Background:

  • Amyloids are cross-β-sheet proteins implicated in human diseases and bacterial biofilm formation.
  • Human amyloids can activate the NLRP3 inflammasome, leading to inflammation.
  • Bacterial amyloids' role in inflammasome activation was previously unclear.

Purpose of the Study:

  • To investigate the activation of the NLRP3 inflammasome by bacterial amyloids.
  • To elucidate the mechanism of NLRP3 inflammasome activation by bacterial amyloids.
  • To determine if bacterial amyloid-induced inflammasome activation causes cell death.

Main Methods:

  • Utilized curli fibers from Salmonella Typhimurium and E. coli.
  • Assessed NLRP3 inflammasome activation and IL-1β production.
  • Investigated the role of Toll-like receptor 2 (TLR2) in the activation pathway.

Main Results:

  • Curli fibers activate the NLRP3 inflammasome, leading to caspase 1 activation and IL-1β production.
  • Toll-like receptor 2 (TLR2) activation by curli fibers is crucial for IL-1β generation.
  • Activation of NLRP3 inflammasome by curli fibers or amyloid β does not cause macrophage cell death.

Conclusions:

  • Bacterial amyloids, specifically curli fibers, activate the NLRP3 inflammasome.
  • A critical cross-talk exists between TLR2 and NLRP3 pathways in response to bacterial amyloids.
  • IL-1β is a key product of the interaction between bacterial amyloids and the innate immune system.

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