ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Protective role of commensals against Clostridium difficile infection via an IL-1β-mediated positive-feedback loop.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
94 citing papers in PubMed, 130 citations in OpenAlex.
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- Immune Aspects of Clostridioides difficile Infection and Vaccine Development.Infectious disease clinics of North America · 2025Review
- The monoclonal antibody AZD5148 confers broad protection against TcdB-diverse Clostridioides difficile strains in mice.PLoS pathogens · 2025Article
- The interplay between host immunity andmBio · 2025Review
- Cellular Solutions: Evaluating Single-Cell Proteins as Sustainable Feed Alternatives in Aquaculture.Biology · 2025Review
- Therapeutic activation of IL-22-producing innate lymphoid cells enhances host defenses to Clostridioides difficile infection.Cell reports · 2025Article
- Fiber- and acetate-mediated modulation of MHC-II expression on intestinal epithelium protects from Clostridioides difficile infection.Cell host & microbe · 2025Article
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- NKp46Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Purified CDT toxins and a clean deletion within the CDT locus provide novel insights into the contribution of binary toxin in cellular inflammation and Clostridioides difficile infection.PLoS pathogens · 2024Article
- Reviewing theMicroorganisms · 2024Review
- Identifying microbiota community patterns important for plant protection using synthetic communities and machine learning.Nature communications · 2023Article
- Host Immune Responses toTropical medicine and infectious disease · 2023Review
- Butyrate Protects against Clostridium difficile Infection by Regulating Bile Acid Metabolism.Microbiology spectrum · 2023Article
- Returning to Nature for the Next Generation of Antimicrobial Therapeutics.Antibiotics (Basel, Switzerland) · 2023Review
- Association of Single Nucleotide Polymorphisms in Nucleotide-Binding Domain Leucine-Rich Repeat Protein 1 withInfection and drug resistance · 2023Article
34 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
6 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile is a Gram-positive obligate anaerobic pathogen that causes pseudomembranous colitis in antibiotic-treated individuals. Commensal bacteria are known to have a significant role in the intestinal accumulation of C. difficile after antibiotic treatment, but little is known about how they affect host immunity during C. difficile infection. In this article, we report that C. difficile infection results in translocation of commensals across the intestinal epithelial barrier that is critical for neutrophil recruitment through the induction of an IL-1β-mediated positive-feedback loop. Mice lacking ASC, an essential mediator of IL-1β and IL-18 processing and secretion, were highly susceptible to C. difficile infection. ASC(-/-) mice exhibited enhanced translocation of commensals to multiple organs after C. difficile infection. Notably, ASC(-/-) mice exhibited impaired CXCL1 production and neutrophil influx into intestinal tissues in response to C. difficile infection. The impairment in neutrophil recruitment resulted in reduced production of IL-1β and CXCL1 but not IL-18. Importantly, translocated commensals were required for ASC/Nlrp3-dependent IL-1β secretion by neutrophils. Mice lacking IL-1β were deficient in inducing CXCL1 secretion, suggesting that IL-1β is the dominant inducer of ASC-mediated CXCL1 production during C. difficile infection. These results indicate that translocated commensals play a crucial role in CXCL1-dependent recruitment of neutrophils to the intestine through an IL-1β/NLRP3/ASC-mediated positive-feedback mechanism that is important for host survival and clearance of translocated commensals during C. difficile infection.
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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.