ArticleInfection and immunity2014
Signaling via tumor necrosis factor receptor 1 but not Toll-like receptor 2 contributes significantly to hydrosalpinx development following Chlamydia muridarum infection.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Infectivity of a pathogenicity-attenuatedInfection and immunity · 2025Article
- Gut dysbiosis contributes to chlamydial induction of hydrosalpinx in the upper genital tract.Frontiers in microbiology · 2023Article
- Article
- Characterization of Pathogenic CD8Infection and immunity · 2022Article
- Reduced Uterine Tissue Damage during Chlamydia muridarum Infection in TREM-1,3-Deficient Mice.Infection and immunity · 2021Article
- Gastrointestinal Chlamydia-Induced CD8Infection and immunity · 2021Article
- Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor.Nature communications · 2021Article
- Tumor Necrosis Factor Alpha-Induced Interleukin-1 Alpha Synthesis and Cell Death Is Increased in Mouse Epithelial Cells Infected With Chlamydia muridarum.The Journal of infectious diseases · 2021Article
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- Endocervical miRNA Expression Profiles in Women Positive for Chlamydia trachomatis with Clinical Signs and/or Symptoms Are Distinct from Those in Women Positive for Chlamydia trachomatis without Signs and Symptoms.Infection and immunity · 2020Article
- Suppression of Chlamydial Pathogenicity by Nonspecific CD8Infection and immunity · 2020Article
- [Role of tumor necrosis factor-α inNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Gastrointestinal Coinfection Promotes Chlamydial Pathogenicity in the Genital Tract.Infection and immunity · 2020Article
- Article
- Chlamydia Spreading from the Genital Tract to the Gastrointestinal Tract - A Two-Hit Hypothesis.Trends in microbiology · 2018Review
- IL-6-mediated signaling pathways limit Chlamydia muridarum infection and exacerbate its pathogenicity in the mouse genital tract.Microbes and infection · 2017Article
- Chlamydial Plasmid-Dependent Pathogenicity.Trends in microbiology · 2017Review
- MicroRNAs Modulate Pathogenesis Resulting from Chlamydial Infection in Mice.Infection and immunity · 2017Article
- TLR2, TLR4 and TLR9 genotypes and haplotypes in the susceptibility to and clinical course of Chlamydia trachomatis infections in Dutch women.Pathogens and disease · 2016Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Chlamydial infection in the lower genital tract can lead to hydrosalpinx, which is accompanied by activation of both pattern recognition receptor TLR2- and inflammatory cytokine receptor TNFR1-mediated signaling pathways. In the current study, we compared the relative contributions of these two receptors to chlamydial induction of hydrosalpinx in mice. We found that mice with or without deficiencies in TLR2 or TNFR1 displayed similar time courses of live organism shedding from vaginal swabs, suggesting that these receptor-mediated signaling pathways are not required for controlling chlamydial lower genital infection. However, mice deficient in TNFR1 but not TLR2 developed significantly reduced hydrosalpinx. The decreased pathogenicity correlated with a significant reduction in interleukin-17 by in vitro-restimulated splenocytes of TNFR1-deficient mice. Although TLR2-deficient mice developed hydrosalpinx as severe as that of wild-type mice, peritoneal macrophages from mice deficient in TLR2 but not TNFR1 produced significantly reduced cytokines upon chlamydial stimulation, suggesting that reduced macrophage responses to chlamydial infection do not always lead to a reduction in hydrosalpinx. Thus, we have demonstrated that the signaling pathways triggered by the cytokine receptor TNFR1 play a more significant role in chlamydial induction of hydrosalpinx than those mediated by the pattern recognition receptor TLR2, which has laid a foundation for further revealing the chlamydial pathogenic mechanisms.
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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.