ArticleThe Journal of biological chemistry2010
cPLA2 regulates the expression of type I interferons and intracellular immunity to Chlamydia trachomatis.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Interferon-λ4 is a cell-autonomous type III interferon associated with pre-treatment hepatitis C virus burden.Virology · 2015Trial
- Chlamydia trachomatis disrupts host metabolism in primary cervical epithelial cells.World journal of microbiology & biotechnology · 2025Article
- Bacteria-Mediated Oncogenesis and the Underlying Molecular Intricacies: What We Know So Far.Frontiers in oncology · 2022Review
- Integrating lncRNAs and mRNAs Expression Profiles in Penicillin-Induced Persistent Chlamydial Infection in HeLa Cells.Frontiers in molecular biosciences · 2022Article
- Expression of oncogenic HRAS in human Rh28 and RMS-YM rhabdomyosarcoma cells leads to oncogene-induced senescence.Scientific reports · 2021Article
- Article
- Lipid Droplet, a Key Player in Host-Parasite Interactions.Frontiers in immunology · 2018Review
- Phosphatidylserine decarboxylase CT699, lysophospholipid acyltransferase CT775, and acyl-ACP synthase CT776 provide membrane lipid diversity to Chlamydia trachomatis.Scientific reports · 2017Article
- Mito-xenophagic killing of bacteria is coordinated by a metabolic switch in dendritic cells.Scientific reports · 2017Article
- Bacterial RNA as a signal to eukaryotic cells as part of the infection process.Discoveries (Craiova, Romania) · 2016Review
- Article
- Role of STAT1 in Chlamydia-Induced Type-1 Interferon Production in Oviduct Epithelial Cells.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Article
- Chlamydia trachomatis Relies on Autonomous Phospholipid Synthesis for Membrane Biogenesis.The Journal of biological chemistry · 2015Article
- STIM1 Is a Novel Component of ER-Chlamydia trachomatis Inclusion Membrane Contact Sites.PloS one · 2015Article
- The type III secretion system (T3SS) of Chlamydophila psittaci is involved in the host inflammatory response by activating the JNK/ERK signaling pathway.BioMed research international · 2015Article
- A dual character of flavonoids in influenza A virus replication and spread through modulating cell-autonomous immunity by MAPK signaling pathways.Scientific reports · 2014Article
- Type II fatty acid synthesis is essential for the replication of Chlamydia trachomatis.The Journal of biological chemistry · 2014Article
- Chlamydial intracellular survival strategies.Cold Spring Harbor perspectives in medicine · 2013Review
- Article
- Phospholipase A2 enzymes: physical structure, biological function, disease implication, chemical inhibition, and therapeutic intervention.Chemical reviews · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Infection with the obligate bacterial intracellular pathogen Chlamydia trachomatis leads to the sustained activation of the small GTPase RAS and many of its downstream signaling components. In particular, the mitogen-activated protein kinase ERK and the calcium-dependent phospholipase cPLA(2) are activated and are important for the onset of inflammatory responses. In this study we tested if activation of ERK and cPLA(2) occurred as a result of RAS signaling during infection and determined the relative contribution of these signaling components to chlamydial replication and survival. We provide genetic and pharmacological evidence that during infection RAS, ERK, and, to a lesser extent, cPLA(2) activation are uncoupled, suggesting that Chlamydia activates individual components of this signaling pathway in a non-canonical manner. In human cell lines, inhibition of ERK or cPLA(2) signaling did not adversely impact C. trachomatis replication. In contrast, in murine cells, inhibition of ERK and cPLA(2) played a significant protective role against C. trachomatis. We determined that cPLA(2)-deficient murine cells are permissive for C. trachomatis replication because of their impaired expression of beta interferon and the induction of immunity-related GTPases (IRG) important for the containment of intracellular pathogens. Furthermore, the MAPK p38 was primarily responsible for cPLA(2) activation in Chlamydia-infected cells and IRG expression. Overall, these findings define a previously unrecognized role for cPLA(2) in the induction of cell autonomous cellular immunity to Chlamydia and highlight the many non-canonical signaling pathways engaged during 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.