ArticleCell & bioscience2018
Heat shock protein 70 protects mouse against post-infection irritable bowel syndrome via up-regulating intestinal γδ T cell's Th17 response.
Article in Cell & bioscience, 2018. 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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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Adenosine 2A receptor contributes to the facilitation of post-infectious irritable bowel syndrome by γδ T cellsWorld journal of gastroenterology · 2023Article
- Upregulated adenosine 2A receptor accelerates post-infectious irritable bowel syndrome by promoting CD4+ T cells' T helper 17 polarization.World journal of gastroenterology · 2022Article
- Increased Vδ1γδT cells predominantly contributed to IL-17 production in the development of adult human post-infectious irritable bowel syndrome.BMC gastroenterology · 2021Article
- The Flavonoid Kurarinone Regulates Macrophage Functions via Aryl Hydrocarbon Receptor and Alleviates Intestinal Inflammation in Irritable Bowel Syndrome.Journal of inflammation research · 2021Article
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Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study investigated the role of HSP70 in modulating intestinal γδ T cells' Th17 response in
methodsThe intestinal HSP70's expression and mRNA level were measured by Western blot and RT-PCR. The intestinal γδ T cell's morphological changes were analyzed using immunofluorescence staining and confocal laser scanning microscope. The pro-inflammatory cytokines' level was detected by ELISA. The isolated and purified γδ T cells were pre-incubated with HSP70 and their functions including proliferation, apoptosis, activation and production of IL-17 were also detected.
resultsHeat treatment augmented intestinal HSP70 expression and alleviated the clinical presentations in PI-IBS mice. Meanwhile, intestinal γδ T cells and local IL-17 level were increased by pre-induction of HSP70. HSP70 promoted the proliferation of PI-IBS mice's intestinal γδ T cells, inhibited the apoptosis and stimulated these cells to secret IL-17 rather than IFN-γ.
conclusionOur results suggest that HSP70 plays a protective role via up-regulating intestinal γδ T cell's Th17 response in PI-IBS mice.
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Registered trials
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