ArticlePloS one2011
Caspase-1 dependent IL-1β secretion is critical for host defense in a mouse model of Chlamydia pneumoniae lung infection.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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
71 citing papers in PubMed, 117 citations in OpenAlex.
- Immunopathogenesis and Cytokine Pathways in Reactive Infectious Mucocutaneous Eruption (RIME) in Pediatric Population: Infectious Triggers and Molecular Insights.Clinical reviews in allergy & immunology · 2026Review
- Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina.Nature communications · 2026Article
- Disproportionality Analysis of Adverse Events Associated with IL-1 Inhibitors in the FDA Adverse Event Reporting System (FAERS).Pharmaceuticals (Basel, Switzerland) · 2025Article
- Treponema denticola major surface protein (Msp): a key player in periodontal pathogenicity and immune evasion.Archives of microbiology · 2025Review
- Sex-dependent vulnerability for Wistar rats model following intranasal instillation with Klebsiella pneumoniae ATCC 43816 causing lobar pneumonia.Pneumonia (Nathan Qld.) · 2024Article
- Two-pore potassium channel TREK-1 (K2P2.1) regulates NLRP3 inflammasome activity in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Review
- Past Exposure to Cigarette Smoke Aggravates Cognitive Impairment in a Rat Model of Vascular Dementia via Neuroinflammation.Cellular and molecular neurobiology · 2022Article
- Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor.Nature communications · 2021Article
- FXR/TGR5 mediates inflammasome activation and host resistance to bacterial infection.Biochemistry and biophysics reports · 2021Article
- Oxidative Stress and Inflammation in SARS-CoV-2- andBiomedicines · 2021Review
- The Purinergic P2X7 Receptor-NLRP3 Inflammasome Pathway: A New Target in Alcoholic Liver Disease?International journal of molecular sciences · 2021Review
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Insights Into Host Cell Cytokines inFrontiers in immunology · 2021Review
- The effects of maternal separation stress experienced by parents on male reproductive potential in the next generation.Heliyon · 2020Article
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- Autophagy Limits Inflammasome DuringFrontiers in immunology · 2019Article
- Cytosolic Recognition of Microbes and Pathogens: Inflammasomes in Action.Microbiology and molecular biology reviews : MMBR · 2018Review
11 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
9 authors at 3 institutions in 1 country.
Funding
Abstract
Chlamydia pneumoniae (CP) is an important human pathogen that causes atypical pneumonia and is associated with various chronic inflammatory disorders. Caspase-1 is a key component of the 'inflammasome', and is required to cleave pro-IL-1β to bioactive IL-1β. Here we demonstrate for the first time a critical requirement for IL-1β in response to CP infection. Caspase-1⁻/⁻ mice exhibit delayed cytokine production, defective clearance of pulmonary bacteria and higher mortality in response to CP infection. Alveolar macrophages harbored increased bacterial numbers due to reduced iNOS levels in Caspase-1⁻/⁻ mice. Pharmacological blockade of the IL-1 receptor in CP infected wild-type mice phenocopies Caspase-1-deficient mice, and administration of recombinant IL-1β rescues CP infected Caspase-1⁻/⁻ mice from mortality, indicating that IL-1β secretion is crucial for host immune defense against CP lung infection. In vitro investigation reveals that CP-induced IL-1β secretion by macrophages requires TLR2/MyD88 and NLRP3/ASC/Caspase-1 signaling. Entry into the cell by CP and new protein synthesis by CP are required for inflammasome activation. Neither ROS nor cathepsin was required for CP infection induced inflammasome activation. Interestingly, Caspase-1 activation during CP infection occurs with mitochondrial dysfunction indicating a possible mechanism involving the mitochondria for CP-induced inflammasome activation.
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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.