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Updated: May 11, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Human pathogenic fungus Trichophyton schoenleinii activates the NLRP3 inflammasome
Hua Li1, Shuxian Wu, Liming Mao
1College of Life Science, Shandong Normal University, Jinan 250014, China.
Abstract:
The fungus Trichophyton schoenleinii (T. schoenleinii) is the causative agent of Trichophytosis and Tinea favosa of the scalp in certain regions of Eurasia and Africa. Human innate immune system plays an important role in combating with various pathogens including fungi. The inflammasome is one of the most critical arms of host innate immunity, which is a protein complex controlling maturation of IL-1β. To clarify whether T. schoenleinii is able to activate the inflammasome, we analyzed human monocytic cell line THP-1 for IL-1β production upon infection with T. schoenleinii strain isolated from Tinea favosa patients, and rapid IL-1β secretion from THP-1 cells was observed. Moreover, applying competitive inhibitors and gene specific silencing with shRNA, we found that T. schoenleinii induced IL-1β secretion, ASC pyroptosome formation as well as caspase-1 activation were all dependent on NLRP3. Cathepsin B activity, ROS production and K⁺ efflux were required for the inflammasome activation by T. schoenleinii. Our data thus reveal that the NLRP3 inflammasome plays an important role in host defense against T. schoenleinii, and suggest that manipulating NLRP3 signaling can be a novel approach for control of diseases caused by T. schoenleinii infection.
Insights
Trichophyton schoenleinii infection activates the NLRP3 inflammasome in human cells. This innate immune response involves IL-1β secretion, crucial for host defense against T. schoenleinii.
Area of Science:
- Immunology
- Mycology
- Cell Biology
Background:
- The fungus Trichophyton schoenleinii causes scalp infections like Tinea favosa.
- The human innate immune system, including inflammasomes, defends against pathogens.
- Inflammasomes are key protein complexes regulating IL-1β maturation.
Purpose of the Study:
- To investigate if T. schoenleinii activates the inflammasome.
- To identify the specific inflammasome pathway involved in the host response.
Main Methods:
- Infection of human monocytic THP-1 cells with T. schoenleinii.
- Analysis of IL-1β production, ASC pyroptosome formation, and caspase-1 activation.
- Use of competitive inhibitors and shRNA for gene silencing (NLRP3, Cathepsin B).
- Assessment of reactive oxygen species (ROS) and potassium (K⁺) efflux.
Main Results:
- T. schoenleinii rapidly induced IL-1β secretion from THP-1 cells.
- Inflammasome activation (IL-1β, ASC, caspase-1) was dependent on NLRP3.
- Cathepsin B activity, ROS production, and K⁺ efflux were essential for activation.
Conclusions:
- The NLRP3 inflammasome is critical for host defense against T. schoenleinii.
- Targeting NLRP3 signaling may offer a new strategy for treating T. schoenleinii infections.
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