ArticlePLoS pathogens2016
An NK Cell Perforin Response Elicited via IL-18 Controls Mucosal Inflammation Kinetics during Salmonella Gut Infection.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 66 citations in OpenAlex.
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- Spatially resolved single-cell transcriptome analysis of murineGut microbes · 2025Article
- Gasdermin-D pores induce an inactivating caspase-4 cleavage that limits IL-18 production in the intestinal epithelium.Communications biology · 2025Article
- Relaxation of mucosal fibronectin fibers in late gut inflammation following neutrophil infiltration in mice.npj biological physics and mechanics · 2025Article
- Distinct cell death pathways induced by granzymes collectively protect against intestinal Salmonella infection.Mucosal immunology · 2024Article
- Acute Ascaris infection impairs the effector functions of natural killer cells in single and Salmonella co-infected pigs.Scientific reports · 2024Article
- LNCGM1082 in Gut Epithelial Cells Promotes Expulsion of Infected Epithelial Cells and Release of IL-18.ImmunoHorizons · 2024Article
- Apoptotic signaling clears engineeredeLife · 2023Article
- Gut microbiota alteration with growth performance, histopathological lesions, and immune responses inVeterinary and animal science · 2023Article
- Gasdermin D is the only Gasdermin that provides protection against acuteProceedings of the National Academy of Sciences of the United States of America · 2023Article
- FlgM is required to evade NLRC4-mediated host protection against flagellatedInfection and immunity · 2023Article
- Intraluminal neutrophils limit epithelium damage by reducing pathogen assault on intestinal epithelial cells during Salmonella gut infection.PLoS pathogens · 2023Article
- Raw potato starch diet supplement in weaned pigs could reduceFrontiers in veterinary science · 2023Article
- Salmonella enterica Serovar Typhimurium Induces NAIP/NLRC4- and NLRP3/ASC-Independent, Caspase-4-Dependent Inflammasome Activation in Human Intestinal Epithelial Cells.Infection and immunity · 2022Article
- Differential regulation of transcription factor T-bet induction during NK cell development and T helper-1 cell differentiation.Immunity · 2022Article
- Epithelial Pyroptosis in Host Defense.Journal of molecular biology · 2022Review
- Host restriction, pathogenesis and chronic carriage of typhoidal Salmonella.FEMS microbiology reviews · 2021Review
- Epithelium-autonomous NAIP/NLRC4 prevents TNF-driven inflammatory destruction of the gut epithelial barrier in Salmonella-infected mice.Mucosal immunology · 2021Article
- Neutrophil Homeostasis and Emergency Granulopoiesis: The Example of Systemic Juvenile Idiopathic Arthritis.Frontiers in immunology · 2021Review
- Current knowledge and perspectives of potential impacts of Salmonella enterica on the profile of the gut microbiota.BMC microbiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Salmonella Typhimurium (S.Tm) is a common cause of self-limiting diarrhea. The mucosal inflammation is thought to arise from a standoff between the pathogen's virulence factors and the host's mucosal innate immune defenses, particularly the mucosal NAIP/NLRC4 inflammasome. However, it had remained unclear how this switches the gut from homeostasis to inflammation. This was studied using the streptomycin mouse model. S.Tm infections in knockout mice, cytokine inhibition and -injection experiments revealed that caspase-1 (not -11) dependent IL-18 is pivotal for inducing acute inflammation. IL-18 boosted NK cell chemoattractants and enhanced the NK cells' migratory capacity, thus promoting mucosal accumulation of mature, activated NK cells. NK cell depletion and Prf-/- ablation (but not granulocyte-depletion or T-cell deficiency) delayed tissue inflammation. Our data suggest an NK cell perforin response as one limiting factor in mounting gut mucosal inflammation. Thus, IL-18-elicited NK cell perforin responses seem to be critical for coordinating mucosal inflammation during early infection, when S.Tm strongly relies on virulence factors detectable by the inflammasome. This may have broad relevance for mucosal defense against microbial pathogens.
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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.