ArticleInfection and immunity2012
Identifying a role for Toll-like receptor 3 in the innate immune response to Chlamydia muridarum infection in murine oviduct epithelial cells.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- Interferon-β Coordinates Epithelial Immune Networks and Fibrotic Responses DuringbioRxiv : the preprint server for biology · 2026Article
- Toll-like Receptor Expression Patterns in the Female Reproductive Tract of Sheep.Animals : an open access journal from MDPI · 2025Article
- Antibacterial Activity of the p53 Tumor Suppressor Protein-How Strong Is the Evidence?International journal of molecular sciences · 2025Review
- Ovarian sex steroid and epithelial control of immune responses in the uterus and oviduct: human and animal models†.Biology of reproduction · 2024Article
- Type-I Interferon Signaling Protects against Chlamydia trachomatis Infection in the Female Lower Genital Tract.Infection and immunity · 2023Article
- Phenotype ofPathogens (Basel, Switzerland) · 2022Article
- Evidence for cGAS-STING Signaling in the Female Genital Tract Resistance to Chlamydia trachomatis Infection.Infection and immunity · 2022Article
- Article
- T cell responses to Chlamydia.Pathogens and disease · 2021Review
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- A post-invasion role forThe Journal of biological chemistry · 2020Article
- Interferon-γ Possesses Anti-Microbial and Immunomodulatory Activity on aMicroorganisms · 2020Article
- Toll-Like Receptor 3 Deficiency Leads to Altered Immune Responses to Chlamydia trachomatis Infection in Human Oviduct Epithelial Cells.Infection and immunity · 2019Article
- Treatment of Intervertebral Disk Disease by the Administration of mRNA Encoding a Cartilage-Anabolic Transcription Factor.Molecular therapy. Nucleic acids · 2019Article
- TLR3 Deficiency Leads to a Dysregulation in the Global Gene-Expression Profile in Murine Oviduct Epithelial Cells Infected withInternational journal of microbiology and current research · 2019Article
- TLR3 deficiency exacerbates the loss of epithelial barrier function during genital tract Chlamydia muridarum infection.PloS one · 2019Article
- Sex hormones alter the response of Toll-like receptor 3 to its specific ligand in fallopian tube epithelial cells.Clinical and experimental reproductive medicine · 2018Article
- The type I interferon receptor is not required for protection in the Chlamydia muridarum and HSV-2 murine super-infection model.Pathogens and disease · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Because epithelial cells are the major cell type productively infected with Chlamydia during genital tract infections, the overall goal of our research was to understand the contribution of infected epithelial cells to the host defense. We previously showed that Toll-like receptor 3 (TLR3) is the critical pattern recognition receptor in oviduct epithelial (OE) cells that is stimulated during Chlamydia infection, resulting in the synthesis of beta interferon (IFN-β). Here, we present data that implicates TLR3 in the expression of a multitude of other innate-inflammatory immune modulators including interleukin-6 (IL-6), CXCL10, CXCL16, and CCL5. We demonstrate that Chlamydia-induced expression of these cytokines is severely disrupted in TLR3-deficient OE cells, whereas Chlamydia replication in the TLR3-deficient cells is more efficient than in wild-type OE cells. Pretreatment of the TLR3-deficient OE cells with 50 U of IFN-β/ml prior to infection diminished Chlamydia replication and restored the ability of Chlamydia infection to induce IL-6, CXCL10, and CCL5 expression in TLR3-deficient OE cells; however, CXCL16 induction was not restored by IFN-β preincubation. Our findings were corroborated in pathway-focused PCR arrays, which demonstrated a multitude of different inflammatory genes that were defectively regulated during Chlamydia infection of the TLR3-deficient OE cells, and we found that some of these genes were induced only when IFN-β was added prior to infection. Our OE cell data implicate TLR3 as an essential inducer of IFN-β and other inflammatory mediators by epithelial cells during Chlamydia infection and highlight the contribution of TLR3 to the inflammatory cytokine response.
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