ArticleInfection and immunity2015
Guanylate binding proteins enable rapid activation of canonical and noncanonical inflammasomes in Chlamydia-infected macrophages.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed, 141 citations in OpenAlex.
- Gut Dysbiosis Promotes Myocardial Hypertrophy via GBP2b/GBP1 in Chronic Colitis.Circulation research · 2026Article
- Chrysin attenuates diabetes-induced retinal injury by inhibiting microglial GBP3/NLRP3/GSDMD-mediated pyroptosis.Animal models and experimental medicine · 2026Article
- Genetic diversity of collaborative cross mice enables the establishment of a novelInfection and immunity · 2026Article
- An overview of human inflammasomes: Activation and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Article
- Substantially Altered Local and Systemic Immunity in Ischemia-Free Versus Conventional Liver Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- A STAT1-GBP1 axis modulates epithelial proliferation in postpartum breast tissue by repressing CDKI expression.Breast cancer research : BCR · 2025Article
- Article
- From mechanisms to therapies: the multifaceted roles of guanylate-binding protein 2 in immunity, cancer, and beyond.Frontiers in immunology · 2025Review
- Caspase-4/11 promotes hyperlipidemia and chronic kidney disease-accelerated vascular inflammation by enhancing trained immunity.JCI insight · 2024Article
- Insights into Chlamydia Development and Host Cells Response.Microorganisms · 2024Review
- Strategies of bacterial detection by inflammasomes.Cell chemical biology · 2024Review
- Advances in vaccine development for Chlamydia trachomatis.Pathogens and disease · 2024Review
- Restriction and evasion: a review of IFNγ-mediated cell-autonomous defense pathways during genital Chlamydia infection.Pathogens and disease · 2024Review
- Article
- Guanylate-binding protein-5 is involved in inflammasome activation by bacterial DNA but only the cooperation of multiple GBPs accounts for control ofFrontiers in immunology · 2024Article
- TNF licenses macrophages to undergo rapid caspase-1, -11, and -8-mediated cell death that restricts Legionella pneumophila infection.PLoS pathogens · 2023Article
- Regulation of chlamydial colonization by IFNγ delivered via distinct cells.Trends in microbiology · 2023Review
- AIM2 sensors mediate immunity toProceedings of the National Academy of Sciences of the United States of America · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 8 institutions in 3 countries.
Funding
Abstract
Interferon (IFN)-inducible guanylate binding proteins (GBPs) mediate cell-autonomous host resistance to bacterial pathogens and promote inflammasome activation. The prevailing model postulates that these two GBP-controlled activities are directly linked through GBP-dependent vacuolar lysis. It was proposed that the rupture of pathogen-containing vacuoles (PVs) by GBPs destroyed the microbial refuge and simultaneously contaminated the host cell cytosol with microbial activators of inflammasomes. Here, we demonstrate that GBP-mediated host resistance and GBP-mediated inflammatory responses can be uncoupled. We show that PVs formed by the rodent pathogen Chlamydia muridarum, so-called inclusions, remain free of GBPs and that C. muridarum is impervious to GBP-mediated restrictions on bacterial growth. Although GBPs neither bind to C. muridarum inclusions nor restrict C. muridarum growth, we find that GBPs promote inflammasome activation in C. muridarum-infected macrophages. We demonstrate that C. muridarum infections induce GBP-dependent pyroptosis through both caspase-11-dependent noncanonical and caspase-1-dependent canonical inflammasomes. Among canonical inflammasomes, we find that C. muridarum and the human pathogen Chlamydia trachomatis activate not only NLRP3 but also AIM2. Our data show that GBPs support fast-kinetics processing and secretion of interleukin-1β (IL-1β) and IL-18 by the NLRP3 inflammasome but are dispensable for the secretion of the same cytokines at later times postinfection. Because IFN-γ fails to induce IL-1β transcription, GBP-dependent fast-kinetics inflammasome activation can drive the preferential processing of constitutively expressed IL-18 in IFN-γ-primed macrophages in the absence of prior Toll-like receptor stimulation. Together, our results reveal that GBPs control the kinetics of inflammasome activation and thereby shape macrophage responses to Chlamydia infections.
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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.