ArticleJournal of biomedical science2014
Staphylococcal enterotoxin B suppresses Alix and compromises intestinal epithelial barrier functions.
Article in Journal of biomedical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 13 citations in OpenAlex.
- A Higher Dose ofToxins · 2023Article
- LncRNA446 Regulates Tight Junctions by Inhibiting the Ubiquitinated Degradation of Alix after Porcine Epidemic Diarrhea Virus Infection.Journal of virology · 2023Article
- Insights into the function of ESCRT and its role in enveloped virus infection.Frontiers in microbiology · 2023Review
- Calu-3 epithelial cells exhibit different immune and epithelial barrier responses from freshly isolated primary nasal epithelial cells in vitro.Clinical and translational allergy · 2018Article
- Alix-mediated assembly of the actomyosin-tight junction polarity complex preserves epithelial polarity and epithelial barrier.Nature communications · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe epithelial barrier dysfunction plays a critical role in the pathogenesis of a broad array of immune diseases. Alix protein is involved in the endolysosome system. This study aims to elucidate the role of Alix in the maintenance of epithelial barrier function.
resultsThe results showed that Alix was detected in T84 cells at both mRNA and protein levels. Exposure to Staphylococcal enterotoxin B (SEB) markedly suppressed the expression of Alix in T84 cells, which could be blocked by knocking down the Toll like receptor 2. The exposure to SEB did not affect the TER, but markedly increased the permeability of T84 monolayers to OVA; the OVA passing through T84 monolayers still preserved the antigenicity manifesting inducing antigen specific T cells proliferation.
conclusionsAlix protein plays a critical role in the maintenance of the barrier function of T84 monolayers.
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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.