Deletion of Nlrp3 protects from inflammation-induced skeletal muscle atrophy
Open accessAbstract
BACKGROUND: Critically ill patients develop atrophic muscle failure, which increases morbidity and mortality. Interleukin-1β (IL-1β) is activated early in sepsis. Whether IL-1β acts directly on muscle cells and whether its inhibition prevents atrophy is unknown. We aimed to investigate if IL-1β activation via the Nlrp3 inflammasome is involved in inflammation-induced atrophy. METHODS: We performed an experimental study and prospective animal trial. The effect of IL-1β on differentiated C2C12 muscle cells was investigated by analyzing gene-and-protein expression, and atrophy response. Polymicrobial sepsis was induced by cecum ligation and puncture surgery in Nlrp3 knockout and wild type mice. Skeletal muscle morphology, gene and protein expression, and atrophy markers were used to analyze the atrophy response. Immunostaining and reporter-gene assays showed that IL-1β signaling is contained and active in myocytes. RESULTS: Immunostaining and reporter gene assays showed that IL-1β signaling is contained and active in myocytes. IL-1β increased Il6 and atrogene gene expression resulting in myocyte atrophy. Nlrp3 knockout mice showed reduced IL-1β serum levels in sepsis. As determined by muscle morphology, organ weights, gene expression, and protein content, muscle atrophy was attenuated in septic Nlrp3 knockout mice, compared to septic wild-type mice 96 h after surgery. CONCLUSIONS: IL-1β directly acts on myocytes to cause atrophy in sepsis. Inhibition of IL-1β activation by targeting Nlrp3 could be useful to prevent inflammation-induced muscle failure in critically ill patients.
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IL-1β and SAA1 signalling converge on NF-κB and increase expression of IL-6.
“Both IL‐1β and SAA1 signalling converge on the transcription factor NF‐ĸB (nuclear factor ‘kappa‐light‐chain‐enhancer’ of activated B‐cells) and increase the expression of interleukin 6 (IL‐6).”
From Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting (2022) · cites this paper as [10]
The Results section ('IL-1β induces myocyte atrophy in vitro'; page unavailable) reports that IL-1β activates NF-κB-dependent signaling and increases Il6 expression in myocytes. The Discussion describes SAA1 as part of a possible inflammatory feedback loop, but does not say that SAA1 activates NF-κB or increases IL-6 expression. The claimed convergence of both signals on NF-κB is therefore not established by this paper. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIL-1β and SAA1 promote muscle atrophy in sepsis, and their inhibition attenuates sepsis-induced muscle atrophy in mice.
“Previously, we reported that interleukin 1β (IL‐1β) 10 and the acute‐phase protein serum amyloid A1 (SAA1) 11 , 12 promote muscle atrophy in sepsis, and that their inhibition attenuated sepsis‐induced muscle atrophy in mice.”
From Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting (2022) · cites this paper as [10]
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Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting
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- Authors
- Huang, N., Kny, M., Riediger, F., Busch, K., Schmidt, S., Luft, F. C., Slevogt, H., & Fielitz, J.
- Affiliations
- Max Delbrück Center (DE)
- Jena University Hospital (DE)
- Corresponding author
- Fielitz, Jens
- Venue
- Intensive Care Medicine Experimental
- Published
- 2017-01-17
- Volume
- 5
- Issue
- 1
- Pages
- 3-3
- ISSN
- 2197-425X (ISSN-L)
- PMC
- PMC5241267
- OpenAlex
- W2572335401
- Cited by
- 95
- References
- 53
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 11 · 2023: 12 · 2022: 12 · 2021: 17 · 2020: 3 · 2019: 8 · 2018: 6 · 2017: 1
- FWCI
- 2.01
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Intensive Care Medicine Experimental (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (acceptedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (FI 965/4-1, FI 965/5-1)
- Grimmke Stiftung
- Experimental and Clinical Research Center
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Intensive Care Unit Cognitive Disorders
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Keywords
- NLRP3 inflammasome, IL-1β, skeletal muscle atrophy, sepsis, polymicrobial sepsis, cecal ligation and puncture, interleukin-6, critically ill patients, muscle failure, NLRP3 knockout mice
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