ArticleAnaerobe2024
IL-13 protects from Clostridioides difficile colitis.
Article in Anaerobe, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Balancing act of cytokines in controlling the severity ofInfection and immunity · 2026Review
- A fully human streptolysin O-neutralizing monoclonal antibody improves survival in a murine model of group A streptococcus necrotizing soft tissue infection.Antimicrobial agents and chemotherapy · 2026Article
- High-fat diet rewires gut host-microbiota relationship to derive worse outcomes followingbioRxiv : the preprint server for biology · 2026Article
- Multiomic Integration Reveals Taxonomic Shifts Correlate to Serum Cytokines in an Antibiotics Model of Gut Microbiome Disruption.Cellular and molecular bioengineering · 2025Article
- Citrobacter rodentium infection activates colonic lamina propria group 2 innate lymphoid cells.PLoS pathogens · 2025Article
- Standard mouse diets lead to differences in severity in infectious and non-infectious colitis.mBio · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectivesClostridioides difficile infection (CDI) is the leading hospital-acquired infection in North America. We have previously discovered that antibiotic disruption of the gut microbiota decreases intestinal IL-33 and IL-25 and increases susceptibility to CDI. We further found that IL-33 promotes protection through type 2 Innate Lymphoid Cells (ILC2s), which produce IL-13. However, the contribution of IL-13 to disease has never been explored.
methodsWe used a validated model of CDI in mice, in which we neutralized via blocking antibodies, or administered recombinant protein, IL-13 to assess the role of this cytokine during infection using weight and clinical scores. Fluorescent activated cell sorting (FACS) was used to characterize myeloid cell population changes in response to IL-13 manipulation.
resultsWe found that administration of IL-13 protected, and anti-IL-13 exacerbated CDI. Additionally, we observed alterations to the monocyte/macrophage cells following neutralization of IL-13 as early as day three post infection. We also observed elevated accumulation of myeloid cells by day four post-infection following IL-13 neutralization. Neutralization of the decoy receptor, IL-13Rα2, resulted in protection from disease, likely through increased available endogenous IL-13.
conclusionsOur data highlight the protective role of IL-13 in protecting from more severe CDI and the association of poor responses with a dysregulated monocyte-macrophage compartment. These results increase our understanding of type 2 immunity in CDI and may have implications for treating disease in patients.
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