ArticleJournal of cardiovascular development and disease2023
Hypertonic Salt Solution Enhances Inflammatory Responses in Cultured Splenic T-Cells from Dahl Salt-Sensitive Rats but Not Dahl Salt-Resistant Rats.
Article in Journal of cardiovascular development and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Immunological insights into hypertension: unraveling triggers and potential therapeutic avenues.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Unraveling the gut microbiota's role in salt-sensitive hypertension: current evidences and future directions.Frontiers in cardiovascular medicine · 2024Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
This study aimed to delineate the effect of sodium chloride on the induction of inflammatory responses and the development of hypertension in Dahl salt-sensitive (SS) and salt-resistant (SR) rats. Splenocytes were isolated from the spleens of SS and SR rats, and cultured on anti-CD3-coated plates for 5 days. The cultured splenic T-cells were challenged with a hypertonic salt solution (0, 20, or 40 mM) in the absence or presence of IL-6 (0, 20, or 60 ng/mL), TGF-β (0, 5, or 15 ng/mL), or IL-23 (0, 10, or 30 ng/mL), and analyzed via ELISA, flow cytometry, and immunofluorescence. The hypertonic salt solution potentiated IL-17A production, as well as the differentiation of Th17 cells via IL-6/TGF-β/IL-23, exclusively in SS rats. However, it did not affect IL-10 production or the differentiation of Treg cells in any of the groups. Furthermore, it potentiated the signal of RORγt in IL-6-treated splenic T-cells from SS rats. To summarize, cultured splenic T-cells exhibited enhanced inflammatory responses on exposure to a hypertonic salt solution in SS rats only, which indicated that sodium chloride and inflammatory cytokines synergistically drove the induction of pathogenic Th17 cells and the development of hypertension in this group only.
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Registered trials
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