ArticleInflammation2018
Fungal β-Glucan Activates the NLRP3 Inflammasome in Human Bronchial Epithelial Cells Through ROS Production.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation.Toxics · 2026Review
- Gut microbiota and its derived metabolites as silent sculptors of non-alcoholic fatty liver disease development and potential guide for non-invasive clinical diagnostics.Molecular biology reports · 2025Review
- Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Article
- Caveolin-1 gene therapy inhibits inflammasome activation to protect from bleomycin-induced pulmonary fibrosis.Scientific reports · 2019Article
- Pathogenic Fungal Infection in the Lung.Frontiers in immunology · 2019Review
- Cytosolic Recognition of Microbes and Pathogens: Inflammasomes in Action.Microbiology and molecular biology reviews : MMBR · 2018Review
- The inflammasomes, immune guardians at defence barriers.Immunology · 2018Review
- Luteoloside Inhibits Proliferation and Promotes Intrinsic and Extrinsic Pathway-Mediated Apoptosis Involving MAPK and mTOR Signaling Pathways in Human Cervical Cancer Cells.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
The nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome has developed as an important bridge between innate immune and infection recently, and has the ability to drive proteolytic procaspase-1 into bioactive caspase-1, then responsible for proteolytic processing of inflammatory cytokines IL-1β and IL-18. Fungal β-glucan, a major component of fungal cell wall, triggers inflammatory response in multiple immune cells, but rarely described in epithelial cells. Also, the relationship between fungal β-glucan and NLRP3 inflammasome is not clear yet. In this study, we first identified that curdlan, a large particulate β-glucan, could activate the NLRP3 inflammasome in LPS-primed human bronchial epithelial cells (HBECs). RT-PCR and Western Blot showed that curdlan upregulate the mRNA as well as intracellular protein expression of NLRP3 and IL-1β in HBECs, along with the activity of caspase-1, and the level of mature IL-1β in cell supernatants was higher by ELISA detection. Further studies demonstrated that the activation of NLRP3 inflammasome could be attenuated by NAC, an inhibitor of ROS. Thus, it indicated curdlan activate NLRP3 inflammasome through a pathway requiring ROS production in HBECs. These findings may provide a new therapeutic target, NLRP3 inflammasome, in invasive pulmonary fungal infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.