ArticleInfection and immunity2005
The innate immune system is activated by stimulation of vaginal epithelial cells with Staphylococcus aureus and toxic shock syndrome toxin 1.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 107 citations in OpenAlex.
- Observations on emergence of mannitol-use-deficientMicrobiology spectrum · 2026Article
- Antifungal, antibacterial, and anti-inflammatory activity of glycerol dithionomonolaurate, an analog of glycerol monolaurate.mSphere · 2025Article
- Pro-inflammatory secreted virulence factors ofASM case reports · 2025Article
- Inhibition of Toxic Shock Syndrome-AssociatedMicrobiology spectrum · 2023Article
- Superantigens, a Paradox of the Immune Response.Toxins · 2022Review
- Comparison of Transcriptional Signatures of Three Staphylococcal Superantigenic Toxins in Human Melanocytes.Biomedicines · 2022Article
- Pathogen Stimulation of Interleukin-8 from Human Vaginal Epithelial Cells through CD40.Microbiology spectrum · 2022Article
- Article
- Human Keratinocyte Response to Superantigens.mSphere · 2020Article
- Device-Associated Menstrual Toxic Shock Syndrome.Clinical microbiology reviews · 2020Review
- The Role of Macrophages inFrontiers in immunology · 2020Review
- Glycerol Monolaurate Contributes to the Antimicrobial and Anti-inflammatory Activity of Human Milk.Scientific reports · 2019Article
- Staphylococcal Superantigens Stimulate Epithelial Cells through CD40 To Produce Chemokines.mBio · 2019Article
- Article
- Cas9 Contributes to Group B Streptococcal Colonization and Disease.Frontiers in microbiology · 2019Article
- Manipulation of Innate and Adaptive Immunity by Staphylococcal Superantigens.Pathogens (Basel, Switzerland) · 2018Review
- The Superantigen Toxic Shock Syndrome Toxin 1 Alters Human Aortic Endothelial Cell Function.Infection and immunity · 2018Article
- Article
- Staphylococcal Superantigens Spark Host-Mediated Danger Signals.Frontiers in immunology · 2016Review
- Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Despite knowledge of the effects of toxic shock syndrome (TSS) toxin 1 (TSST-1) on the adaptive immune system, little is known about stimulation of the innate immune system, particularly epithelial cells. This study investigated the interactions of TSS Staphylococcus aureus and TSST-1 with human vaginal epithelial cells (HVECs) and porcine mucosal surfaces. When cocultured with HVECs for 6 h, TSS S. aureus MN8 proliferated, formed aggregates on the HVEC surfaces, and produced exotoxins. Receptor binding studies showed that 35S-TSST-1 bound to 5 x 10(4) receptors per HVEC, with saturation at 15 min. Affymetrix Human GeneChip U133A microarray analysis determined S. aureus MNSM (100 bacteria/HVEC) caused at least twofold up- or down-regulation of 410 HVEC genes by 6 h; these data were also confirmed with S. aureus MN8. TSST-1 (100 microg/ml) caused up- or down-regulation of 2,386 HVEC genes by 6 h. In response to S. aureus, the HVEC genes most up-regulated compared to those in controls were those coding for chemokines or cytokines--MIP-3alpha, 478-fold; GRO-alpha, 26-fold; GRO-beta, 14-fold; and GRO-gamma, 30-fold--suggesting activation of innate immunity. TSST-1 also caused up-regulation of chemokine/cytokine genes. Chemokine/cytokine gene up-regulation was confirmed by enzyme-linked immunosorbent assays measuring the corresponding proteins induced by S. aureus and TSST-1. S. aureus MN8, when incubated with porcine vaginal tissue, increased the flux of 35S-TSST-1 across the mucosal surface. This was accompanied by influx of lymphocytes into the upper layers of the tissue. These data suggest innate immune system activation through epithelial cells, reflected in chemokine/cytokine production and influx of lymphocytes, may cause changes in vaginal mucosa permeability, facilitating TSST-1 penetration.
Indexed as
Identifiers
What OpenQuestion holds
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.