ArticlePLoS pathogens2011
Chlamydia trachomatis co-opts the FGF2 signaling pathway to enhance infection.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- Emerging Insights into Protein Post-Translational Modifications in Chlamydia-Host Interactions.The American journal of pathology · 2025Review
- 3-O Sulfated Heparan Sulfate (G2) Peptide Ligand Impairs the Infectivity ofBiomolecules · 2025Article
- Sulfated Glycosaminoglycans as Inhibitors for Chlamydia Infections: Molecular Weight and Sulfation Dependence.Macromolecular bioscience · 2025Article
- Chlamydia trachomatis invasion: a duet of effectors.Biochemical Society transactions · 2025Review
- Infection of human organoids supports an intestinal niche for Chlamydia trachomatis.PLoS pathogens · 2024Article
- Insights into Chlamydia Development and Host Cells Response.Microorganisms · 2024Review
- Intracellular lifestyle of Chlamydia trachomatis and host-pathogen interactions.Nature reviews. Microbiology · 2023Review
- Establishing the intracellular niche of obligate intracellular vacuolar pathogens.Frontiers in cellular and infection microbiology · 2023Review
- Distinct roles of the Chlamydia trachomatis effectors TarP and TmeA in the regulation of formin and Arp2/3 during entry.Journal of cell science · 2022Article
- Galectins as potential therapeutic targets in STIs in the female genital tract.Nature reviews. Urology · 2022Review
- The Chlamydia trachomatis Tarp effector targets the Hippo pathway.Biochemical and biophysical research communications · 2021Article
- Cathelicidin ΔPb-CATH4 derived from Python bivittatus accelerates the healing of Staphylococcus aureus-infected wounds in mice.Amino acids · 2021Article
- Hijacking and Use of Host Kinases by Chlamydiae.Pathogens (Basel, Switzerland) · 2020Review
- Lipid rafts and pathogens: the art of deception and exploitation.Journal of lipid research · 2020Review
- Epidermal Growth Factor Receptor and Transforming Growth Factor β Signaling Pathways Cooperate To MediateInfection and immunity · 2020Article
- Pathogenic Puppetry: Manipulation of the Host Actin Cytoskeleton byInternational journal of molecular sciences · 2019Review
- A Chlamydia pneumoniae adhesin induces phosphatidylserine exposure on host cells.Nature communications · 2019Article
- Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane reveals functional interactions with endoplasmic reticulum exit sites.PLoS pathogens · 2019Article
- A FACS-Based Genome-wide CRISPR Screen Reveals a Requirement for COPI in Chlamydia trachomatis Invasion.iScience · 2019Article
- Chlamydial Infection From Outside to Inside.Frontiers in microbiology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The molecular details of Chlamydia trachomatis binding, entry, and spread are incompletely understood, but heparan sulfate proteoglycans (HSPGs) play a role in the initial binding steps. As cell surface HSPGs facilitate the interactions of many growth factors with their receptors, we investigated the role of HSPG-dependent growth factors in C. trachomatis infection. Here, we report a novel finding that Fibroblast Growth Factor 2 (FGF2) is necessary and sufficient to enhance C. trachomatis binding to host cells in an HSPG-dependent manner. FGF2 binds directly to elementary bodies (EBs) where it may function as a bridging molecule to facilitate interactions of EBs with the FGF receptor (FGFR) on the cell surface. Upon EB binding, FGFR is activated locally and contributes to bacterial uptake into non-phagocytic cells. We further show that C. trachomatis infection stimulates fgf2 transcription and enhances production and release of FGF2 through a pathway that requires bacterial protein synthesis and activation of the Erk1/2 signaling pathway but that is independent of FGFR activation. Intracellular replication of the bacteria results in host proteosome-mediated degradation of the high molecular weight (HMW) isoforms of FGF2 and increased amounts of the low molecular weight (LMW) isoforms, which are released upon host cell death. Finally, we demonstrate the in vivo relevance of these findings by showing that conditioned medium from C. trachomatis infected cells is enriched for LMW FGF2, accounting for its ability to enhance C. trachomatis infectivity in additional rounds of infection. Together, these results demonstrate that C. trachomatis utilizes multiple mechanisms to co-opt the host cell FGF2 pathway to enhance bacterial infection and spread.
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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 Socratic graph.