ArticleNature communications2024
IL-17C is a driver of damaging inflammation during Neisseria gonorrhoeae infection of human Fallopian tube.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Distinct central and peripheral airway features in bronchiolitis obliterans and COPD: an observational study.BMC pulmonary medicine · 2026Observational
- The Mucosal Cytokine Landscape of Acute Gonorrhea Using a Controlled Human Infection Model.medRxiv : the preprint server for health sciences · 2026Article
- MtrR Regulates a Major Lytic Transglycosylase (Microorganisms · 2026Article
- Identification of a robust multitarget protein panel for Parkinson's disease via absolute quantification and large-scale external replication.Brain communications · 2026Article
- Role of IL-17 cytokines in tubal fibrosis and infertility due to salpingitis.Molecular biology reports · 2025Review
- Engineered Tissue Models to Decode Host-Microbiota Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Exploring the Association Between Immune Cell Phenotypes and Osteoporosis Mediated by Inflammatory Cytokines: Insights from GWAS and Single-Cell Transcriptomics.ImmunoTargets and therapy · 2025Article
- Sustained STING-IRF7 signaling aggravates LPS-induced endometrial inflammation via excessive neutrophil extracellular traps generation.Frontiers in immunology · 2025Article
- Combined assembloid modeling and 3D whole-organ mapping captures the microanatomy and function of the human fallopian tube.Science advances · 2024Article
- Mutation ofJournal of bacteriology · 2023Article
- Mutation ofbioRxiv : the preprint server for biology · 2023Article
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Authors and funding
6 authors.
Funding
Abstract
The human pathogen Neisseria gonorrhoeae ascends into the upper female reproductive tract to cause damaging inflammation within the Fallopian tubes and pelvic inflammatory disease (PID), increasing the risk of infertility and ectopic pregnancy. The loss of ciliated cells from the epithelium is thought to be both a consequence of inflammation and a cause of adverse sequelae. However, the links between infection, inflammation, and ciliated cell extrusion remain unresolved. With the use of ex vivo cultures of human Fallopian tube paired with RNA sequencing we defined the tissue response to gonococcal challenge, identifying cytokine, chemokine, cell adhesion, and apoptosis related transcripts not previously recognized as potentiators of gonococcal PID. Unexpectedly, IL-17C was one of the most highly induced genes. Yet, this cytokine has no previous association with gonococcal infection nor pelvic inflammatory disease and thus it was selected for further characterization. We show that human Fallopian tubes express the IL-17C receptor on the epithelial surface and that treatment with purified IL-17C induces pro-inflammatory cytokine secretion in addition to sloughing of the epithelium and generalized tissue damage. These results demonstrate a previously unrecognized but critical role of IL-17C in the damaging inflammation induced by gonococci in a human explant model of PID.
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