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Updated: Apr 23, 2026
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Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
Published on: May 21, 2018
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Keeping inflammasomes in check during bone resorption.
Caroline Schmidt1, Ulf Wagner1,2
1Division of Rheumatology, Department of Endocrinology, Nephrology, Rheumatology, Leipzig University, Leipzig, Germany.
Science Signaling
|April 21, 2026
Summary
Osteoclasts prevent inflammasome activation by regulating calcium (Ca2+) influx via Tmem178. This mechanism protects bone from excessive resorption linked to inflammatory signaling.
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Calcium (Ca2+) flux is crucial for NLRP3 inflammasome activation.
- Bone-resorbing osteoclasts exist in a Ca2+-rich milieu during bone resorption.
- Uncontrolled inflammasome activation can exacerbate bone resorption.
Purpose of the Study:
- To investigate how osteoclasts manage Ca2+ levels to prevent inflammasome activation.
- To identify the molecular mechanisms underlying inflammasome regulation in osteoclasts.
- To understand the role of Tmem178 in osteoclast function and bone homeostasis.
Main Methods:
- Analysis of Ca2+ signaling pathways in osteoclasts.
- Investigation of the role of the membrane protein Tmem178.
- Assessment of inflammasome activation markers in osteoclast models.
- Evaluation of bone resorption assays.
Main Results:
- Osteoclasts limit Ca2+ influx through Tmem178 to prevent NLRP3 inflammasome activation.
- Tmem178 acts as a critical regulator of Ca2+ homeostasis in osteoclasts.
- This regulation prevents excessive bone resorption driven by inflammatory signals.
Conclusions:
- Osteoclasts employ Tmem178 to control Ca2+ flux, thereby inhibiting inflammasome activation.
- This finding reveals a novel mechanism for protecting bone from inflammatory damage.
- Targeting Tmem178 could offer therapeutic strategies for bone-related inflammatory diseases.
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