ArticleInfection and immunity2015
Toll-like receptor 2 and NLRP3 cooperate to recognize a functional bacterial amyloid, curli.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
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Who cites it
75 citing papers in PubMed, 116 citations in OpenAlex.
- A Novel Biofilm Amyloid Ligand for Caspase-11 Drives Hyperactivation in Dendritic Cells.bioRxiv : the preprint server for biology · 2026Article
- Salmonella infection and biofilms drive anti-C1q and anti-dsDNA autoantibodies in systemic autoimmunity.PLoS pathogens · 2026Article
- Contribution of localmBio · 2026Article
- Outbreaks of fluconazole-resistant Candida parapsilosis are driven by low-biofilm-producing isolates that emerge under host selection.PLoS biology · 2026Article
- Biofilm-derived curli and Z-DNA shape anti-DNA antibody responses during Salmonella infections.PLoS pathogens · 2026Article
- A Comprehensive Review of the Gut-Microbiota-Brain Axis in Alzheimer's Disease: From Pathophysiology to Potential Therapies.Pathogens (Basel, Switzerland) · 2026Review
- Taxonomic and functional remodeling of the gut microbiota during aging and implications for microbiota-derived biomarkers.World journal of microbiology & biotechnology · 2026Review
- A host anti-amyloidogenic stomach-specific protein inhibits colonization and biofilm formation by adherent invasive Escherichia coli in the colon.Research square · 2026Article
- Biofilm-associated proteins: from the gut biofilms to neurodegeneration.Gut microbes · 2025Review
- Biofilm-associated molecular patterns: BAMPs.Infection and immunity · 2025Review
- Bidirectional crosstalk between the gut microbiota and cellular compartments of brain: Implications for neurodevelopmental and neuropsychiatric disorders.Translational psychiatry · 2025Review
- What would it take to prove that a chronic infection is a causal agent in Alzheimer's disease?Trends in neurosciences · 2025Review
- Review
- Gut Microbiota and Immune System Dynamics in Parkinson's and Alzheimer's Diseases.International journal of molecular sciences · 2024Review
- Lactate promotes the biofilm-to-invasive-planktonic transition inInfection and immunity · 2024Article
- The menace within: bacterial amyloids as a trigger for autoimmune and neurodegenerative diseases.Current opinion in microbiology · 2024Review
- DNA at the center of mammalian innate immune recognition of bacterial biofilms.Trends in immunology · 2024Review
- Frailty and Parkinson's disease: the role of diabetes mellitus.Frontiers in medicine · 2024Review
- Commensal Bacteria Impact on Intestinal Toll-like Receptor Signaling inPathogens (Basel, Switzerland) · 2023Article
- Engineered Curli Nanofilaments as a Self-Adjuvanted Antigen Delivery Platform.Advanced healthcare materials · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloids are proteins with cross-β-sheet structure that contribute to pathology and inflammation in complex human diseases, including Alzheimer's disease, Parkinson's disease, type II diabetes, and secondary amyloidosis. Bacteria also produce amyloids as a component of their extracellular matrix during biofilm formation. Recently, several human amyloids were shown to activate the NLRP3 inflammasome, leading to the activation of caspase 1 and production of interleukin 1β (IL-1β). In this study, we investigated the activation of the NLRP3 inflammasome by bacterial amyloids using curli fibers, produced by Salmonella enterica serovar Typhimurium and Escherichia coli. Here, we show that curli fibers activate the NLRP3 inflammasome, leading to the production of IL-1β via caspase 1 activation. Investigation of the underlying mechanism revealed that activation of Toll-like receptor 2 (TLR2) by curli fibers is critical in the generation of IL-1β. Interestingly, activation of the NLRP3 inflammasome by curli fibers or by amyloid β of Alzheimer's disease does not cause cell death in macrophages. Overall, these data identify a cross talk between TLR2 and NLRP3 in response to the bacterial amyloid curli and generation of IL-1β as a product of this interaction.
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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.