ArticleCellular microbiology2009
A protein secreted by the respiratory pathogen Chlamydia pneumoniae impairs IL-17 signalling via interaction with human Act1.
Article in Cellular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Review
- TheMicrobiology spectrum · 2024Article
- Gut-Lung Microbiota Interaction in COPD Patients: A Literature Review.Medicina (Kaunas, Lithuania) · 2022Review
- Application of aJournal of bacteriology · 2021Article
- Clear Victory forFrontiers in microbiology · 2019Review
- Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies.Journal of immunology research · 2019Review
- The Immunoregulation of Th17 in Host against Intracellular Bacterial Infection.Mediators of inflammation · 2018Review
- The Chlamydia trachomatis type III secretion substrates CT142, CT143, and CT144 are secreted into the lumen of the inclusion.PloS one · 2017Article
- Chlamydia cell biology and pathogenesis.Nature reviews. Microbiology · 2016Review
- Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia.Infection and immunity · 2015Article
- Article
- New frontiers in type III secretion biology: the Chlamydia perspective.Infection and immunity · 2014Review
- IL-17 family: cytokines, receptors and signaling.Cytokine · 2013Review
- Transcription factor complex AP-1 mediates inflammation initiated by Chlamydia pneumoniae infection.Cellular microbiology · 2013Article
- Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- IL-17A and Th17 cells in lung inflammation: an update on the role of Th17 cell differentiation and IL-17R signaling in host defense against infection.Clinical & developmental immunology · 2013Review
- Proof of concept: A bioinformatic and serological screening method for identifying new peptide antigens for Chlamydia trachomatis related sequelae in women.Results in immunology · 2013Article
- Chlamydia pneumoniae-specific IgE is prevalent in asthma and is associated with disease severity.PloS one · 2012Article
- Unity in variety--the pan-genome of the Chlamydiae.Molecular biology and evolution · 2011Article
- Modulation of NF-κB signalling by microbial pathogens.Nature reviews. Microbiology · 2011Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Chlamydia pneumoniae is a common respiratory pathogen that has been associated with a variety of chronic diseases including asthma and atherosclerosis. Chlamydiae are obligate intracellular parasites that primarily infect epithelial cells where they develop within a membrane-bound vacuole, termed an inclusion. Interactions between the microorganism and eukaryotic cell can be mediated by chlamydial proteins inserted into the inclusion membrane. We describe here a novel C. pneumoniae-specific inclusion membrane protein (Inc) CP0236, which contains domains exposed to the host cytoplasm. We demonstrate that, in a yeast two-hybrid screen, CP0236 interacts with the NFκB activator 1 (Act1) and this interaction was confirmed in HeLa 229 cells where ectopically expressed CP0236 was co-immunoprecipitated with endogenous Act1. Furthermore, we demonstrate that Act1 displays an altered distribution in the cytoplasm of HeLa cells infected with C. pneumoniae where it associates with the chlamydial inclusion membrane. This sequestration of Act1 by chlamydiae inhibited recruitment of the protein to the interleukin-17 (IL-17) receptor upon stimulation of C. pneumoniae-infected cells with IL-17A. Such inhibition of the IL-17 signalling pathway led to protection of Chlamydia-infected cells from NFκB activation in IL-17-stimulated cells. We describe here a unique strategy employed by C. pneumoniae to achieve inhibition of NFκB activation via interaction of CP0236 with mammalian Act1.
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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.