ArticleThe Journal of experimental medicine2025
Enteric tuft cell inflammasome activation drives NKp46+ILC3 IL22 via PGD2 and inhibits Salmonella.
Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Host-microbiota-pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis.Nature reviews. Microbiology · 2026Review
- Gastrointestinal tuft cells: Recent insights and next questions.Science immunology · 2026Review
- A Hypothesis of Gut-Liver Mediated Heterosis: Multi-Omics Insights into Hybrid Taimen Immunometabolism (Animals : an open access journal from MDPI · 2025Article
- Intestinal IL-22RA1 signaling regulatesFrontiers in microbiology · 2025Article
- The role of the tuft cell-interleukin-25 axis in the pathogenesis of inflammatory bowel disease.Frontiers in immunology · 2025Review
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Authors and funding
13 authors.
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Abstract
To distinguish pathogens from commensals, the intestinal epithelium employs cytosolic innate immune sensors. Activation of the NAIP-NLRC4 inflammasome initiates extrusion of infected intestinal epithelial cells (IEC) upon cytosolic bacterial sensing. We previously reported that activation of the inflammasome in tuft cells, which are primarily known for their role in parasitic infections, leads to the release of prostaglandin D2 (PGD2). We observe that NAIP-NLRC4 inflammasome activation in tuft cells leads to an antibacterial response with increased IL-22 and antimicrobial protein levels within the small intestine, which is dependent on PGD2 signaling. A NKp46+ subset of ILC3 expresses the PGD2 receptor CRTH2 and is the source of the increased IL-22. Inflammasome activation in tuft cells also leads to better control of Salmonella Typhimurium in the distal small intestine. However, tuft cells in the cecum and colon are dispensable for antibacterial immunity. These data support that intestinal tuft cells can also induce antibacterial responses, possibly in a tissue-specific manner.
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