Affiliation:
1. Department of Pharmacology, School of Medicine, Daegu, 41944, Republic of Korea
2. Cardiovascular Research Institute, Daegu 41944, Republic of Korea
3. BK21 Plus KNU Biomedical Convergence Program, Daegu 41944, Republic of Korea
4. Department of Biomedical Science, The Graduate School, Kyungpook National University, Daegu 41944, Republic of Korea
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.
Funder
National Research Foundation of Korea
Korea Health Industry Development Institute
Subject
Pharmacology (medical),General Pharmacology, Toxicology and Pharmaceutics
Cited by
2 articles.
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