ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Inflammasome activation by Campylobacter jejuni.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. 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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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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Tissue-Resident Macrophages: Linking Physiology and Inflammation in Infection.Clinical reviews in allergy & immunology · 2026Review
- Virulence and Antimicrobial Resistance inAntibiotics (Basel, Switzerland) · 2026Review
- Determinate the effects of Arabic gum and Lactobacillus acidophilus on the gut microbiota ALPK1/NFKB/NLRP6 and NLRP2 signaling pathway and virulence gene profile in rats with Campylobacter jejuni exosome application.Archives of microbiology · 2026Article
- Effect of the polysaccharide capsule and its heptose on the resistance of Campylobacter jejuni to innate immune defenses.MicrobiologyOpen · 2024Article
- Inhibition of the NLRP3 Inflammasome by a Quercus Serrata Extract and Isolation of the Component Compounds for the Treatment of Arthritis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Extremely small and incredibly close: Gut microbes as modulators of inflammation and targets for therapeutic intervention.Frontiers in microbiology · 2022Review
- The ALPK1 pathway drives the inflammatory response to Campylobacter jejuni in human intestinal epithelial cells.PLoS pathogens · 2021Article
- The Host Cellular Immune Response to Infection by Campylobacter Spp. and Its Role in Disease.Infection and immunity · 2021Review
- Article
- OmpA Protein-DeficientPathogens (Basel, Switzerland) · 2021Article
- Campylobacter Virulence Factors and Molecular Host-Pathogen Interactions.Current topics in microbiology and immunology · 2021Review
- Article
- Human Immunity AgainstImmune network · 2019Review
- MUC1 is a receptor for the Salmonella SiiE adhesin that enables apical invasion into enterocytes.PLoS pathogens · 2019Article
- Cytosolic Recognition of Microbes and Pathogens: Inflammasomes in Action.Microbiology and molecular biology reviews : MMBR · 2018Review
- NLRP3 inflammasome pathway has a critical role in the host immunity against clinically relevant Acinetobacter baumannii pulmonary infection.Mucosal immunology · 2018Article
- Treatment with pCramoll Alone and in Combination with Fluconazole Provides Therapeutic Benefits inFrontiers in cellular and infection microbiology · 2017Article
- Baicalin suppresses NLRP3 inflammasome and nuclear factor-kappa B (NF-κB) signaling during Haemophilus parasuis infection.Veterinary research · 2016Article
- Interleukin-18 Mediates Immune Responses to Campylobacter jejuni Infection in Gnotobiotic Mice.PloS one · 2016Article
- Transcriptomic and proteomic analyses reveal key innate immune signatures in the host response to the gastrointestinal pathogen Campylobacter concisus.Infection and immunity · 2015Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The Gram-negative pathogen Campylobacter jejuni is the most common cause of bacterial foodborne disease worldwide. The mechanisms that lead to bacterial invasion of eukaryotic cells and massive intestinal inflammation are still unknown. In this study, we report that C. jejuni infection of mouse macrophages induces upregulation of pro-IL-1β transcript and secretion of IL-1β without eliciting cell death. Immunoblotting indicated cleavage of caspase-1 and IL-1β in infected cells. In bone marrow-derived macrophages from different knockout mice, IL-1β secretion was found to require NLRP3, ASC, and caspase-1/11 but not NLRC4. In contrast to NLRP3 activation by ATP, C. jejuni activation did not require priming of these macrophages. C. jejuni also activated the NLRP3 inflammasome in human macrophages as indicated by the presence of ASC foci and caspase-1-positive cells. Analysis of a vast array of C. jejuni mutants with defects in capsule formation, LPS biosynthesis, chemotaxis, flagella synthesis and flagellin (-like) secretion, type 6 secretion system needle protein, or cytolethal distending toxin revealed a direct correlation between the number of intracellular bacteria and NLRP3 inflammasome activation. The C. jejuni invasion-related activation of the NLRP3 inflammasome without cytotoxicity and even in nonprimed cells extends the known repertoire of bacterial inflammasome activation and likely contributes to C. jejuni-induced intestinal inflammation.
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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.