ArticleMucosal immunology2019
ASC and NLRP3 maintain innate immune homeostasis in the airway through an inflammasome-independent mechanism.
Article in Mucosal immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- KCNJ2 is Required for NLRP3 Inflammasome Activation That Drives Allergic Airway Inflammation and Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A living therapeutic platform for localized in situ modulation of macrophage pyroptosis ameliorates GVHD while preserving GVL.Journal of nanobiotechnology · 2026Article
- Article
- Identification and Validation of FOXK1-Related Biomarkers in Diabetic Retinopathy.International journal of general medicine · 2026Article
- Advances in infection-immunity mechanisms and molecular regulatory networks in severe pneumonia-associated lung injury.Frontiers in immunology · 2026Review
- Systemic inflammation-induced adipose tissue remodeling drives psoriasis exacerbation in obesity through epigenetic and immunometabolic dysregulation.Theranostics · 2025Article
- Pyroptosis-driven immune dysregulation in COPD: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Molecular mechanisms of streptococcal disruption of the blood-brain barrier and their pathogenic role in bacterial meningitis.Frontiers in immunology · 2025Review
- Mass spectrometry-based proteomic exploration of diverse murine macrophage cellular models.Life science alliance · 2025Article
- Arsenic Exposure Induces Neuro-immune Toxicity in the Cerebral Cortex and the Hippocampus via Neuroglia and NLRP3 Inflammasome Activation in C57BL/6 Mice.Biological trace element research · 2024Article
- Cryptotanshinone Inhibits Bladder Cancer Cell Malignant Progression in a Lipopolysaccharide-Induced Inflammatory Microenvironment through NLRP3 Inhibition.Mediators of inflammation · 2024Article
- Diagnostic and Prognostic Value of Serum Omentin-1 in Sepsis: A Prospective Study in Critically Ill Patients.Medicina (Kaunas, Lithuania) · 2023Article
- Role of the caspase-8/RIPK3 axis in Alzheimer's disease pathogenesis and Aβ-induced NLRP3 inflammasome activation.JCI insight · 2023Article
- Activation of the NLRP3 inflammasome by RAC1 mediates a new mechanism in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Hierarchical cell-type-specific functions of caspase-11 in LPS shock and antibacterial host defense.Cell reports · 2021Article
- GABA transporter sustains IL-1β production in macrophages.Science advances · 2021Article
- Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome.Toxins · 2021Article
- Stem Cell-Derived Exosomes Ameliorate Doxorubicin-Induced Muscle Toxicity through Counteracting Pyroptosis.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Neuroinflammation Mediated by NLRP3 Inflammasome After Intracerebral Hemorrhage and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Genetic disruption of the inflammasome adaptor ASC has minimal impact on the pathogenesis of Duchenne muscular dystrophy in mdx mice.Life sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is widely accepted that inflammasomes protect the host from microbial pathogens by inducing inflammatory responses through caspase-1 activation. Here, we show that the inflammasome components ASC and NLRP3 are required for resistance to pneumococcal pneumonia, whereas caspase-1 and caspase-11 are dispensable. In the lung of S. pneumoniae-infected mice, ASC and NLRP3, but not caspase-1/11, were required for optimal expression of several mucosal innate immune proteins. Among them, TFF2 and intelectin-1 appeared to be protective against pneumococcal pneumonia. During infection, ASC and NLRP3 maintained the expression of the transcription factor SPDEF, which can facilitate the expression of the mucosal defense factor genes. Moreover, activation of STAT6, a key regulator of Spdef expression, depended on ASC and NLRP3. Overexpression of these inflammasome proteins sustained STAT6 phosphorylation induced by type 2 cytokines. Collectively, this study suggests that ASC and NLRP3 promote airway mucosal innate immunity by an inflammasome-independent mechanism involving the STAT6-SPDEF pathway.
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