ArticleJournal of immunology (Baltimore, Md. : 1950)2012
NLRC4 inflammasome-mediated production of IL-1β modulates mucosal immunity in the lung against gram-negative bacterial infection.
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 83 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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Who cites it
83 citing papers in PubMed, 126 citations in OpenAlex.
- NLRC4 deficiency improves host protection during sepsis by regulating macrophage and T-cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- NLRP3 inflammasomes at the ARDS-cancer interface: mechanisms and translational hypotheses.Frontiers in immunology · 2026Review
- Toward precision host-directed immunomodulation in community-acquired pneumonia: a proposed endotype-target-natural-product framework and a roadmap for validation in human lung organoids.Frontiers in medicine · 2026Review
- Inflammasomes and autophagy in cancer: unlocking targeted therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Insights into the roles of macrophages in Klebsiella pneumoniae infections: a comprehensive review.Cellular & molecular biology letters · 2025Review
- Review
- Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025Review
- Caspase-11 and NLRP3 exacerbate systemic Klebsiella infection through reducing mitochondrial ROS production.Frontiers in immunology · 2025Article
- Autophagy, cell death, and cytokines inEmerging microbes & infections · 2023Review
- Review
- The influence of pyroptosis-related genes on the development of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2023Article
- Inflammasome-Independent Roles of NLR and ALR Family Members.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Role of toll-like receptors and nod-like receptors in acute lung infection.Frontiers in immunology · 2023Review
- Pyroptosis and pyroptosis-inducing cancer drugs.Acta pharmacologica Sinica · 2022Review
- Klebsiella pneumoniae hijacks the Toll-IL-1R protein SARM1 in a type I IFN-dependent manner to antagonize host immunity.Cell reports · 2022Article
- Prognostic prediction of systemic immune-inflammation status for patients with colorectal cancer: a novel pyroptosis-related model.World journal of surgical oncology · 2022Article
- The Therapeutic Treatment with the GAG-Binding Chemokine Fragment CXCL9(74-103) Attenuates Neutrophilic Inflammation and Lung Dysfunction duringInternational journal of molecular sciences · 2022Article
- The Effect of PGC-1alpha-SIRT3 Pathway Activation onPathogens (Basel, Switzerland) · 2022Article
- Host defense against the infection ofFrontiers in cellular and infection microbiology · 2022Review
- Host Immune Response to Clinical HypervirulentJournal of immunology research · 2022Article
23 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bacterial flagellin is critical to mediate NLRC4 inflammasome-dependent caspase-1 activation. However, Shigella flexneri, a nonflagellated bacterium, and a flagellin (fliC) knockout strain of Pseudomonas aeruginosa are known to activate NLRC4 in bone marrow-derived macrophages. Furthermore, the flagellin-deficient fliC strain of P. aeruginosa was used in a mouse model of peritonitis to show the requirement of NLRC4. In a model of pulmonary P. aeruginosa infection, flagellin was shown to be essential for the induction of NLRC4-dependent caspase-1 activation. Moreover, in all P. aeruginosa studies, IL-1β production was attenuated in NLRC4(-/-) mice; however, the role of IL-1β in NLRC4-mediated innate immunity in the lungs against a nonflagellated bacterium was not explored. In this article, we report that NLRC4 is important for host survival and bacterial clearance, as well as neutrophil-mediated inflammation in the lungs following Klebsiella pneumoniae infection. NLRC4 is essential for K. pneumoniae-induced production of IL-1β, IL-17A, and neutrophil chemoattractants (keratinocyte cell-derived chemokines, MIP-2, and LPS-induced CXC chemokines) in the lungs. NLRC4 signaling in hematopoietic cells contributes to K. pneumoniae-induced lung inflammation. Furthermore, exogenous IL-1β, but not IL-18 or IL-17A, partially rescued survival, neutrophil accumulation, and cytokine/chemokine expression in the lungs of NLRC4(-/-) mice following infectious challenge. Furthermore, IL-1R1(-/-) mice displayed a decrease in neutrophilic inflammation in the lungs postinfection. Taken together, these findings provide novel insights into the role of NLRC4 in host defense against K. pneumoniae 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.