Effect of short-term changes in salt intake on plasma cytokines in women with healthy and hypertensive pregnancies

Sai Sindhu Thangaraj*, Tina Signe Gissel Gunlund, Jane Stubbe, Yaseelan Palarasah, Per Svenningsen, Lise Hald Nielsen, Per Glud Ovesen, Boye L. Jensen

*Kontaktforfatter

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Abstract

Background: Salt (NaCl) promotes T-lymphocyte conversion to pro-inflammatory Th-17 cells in vitro. Interleukin (IL)-17A aggravates hypertension in preeclampsia (PE) models. Objectives: It was hypothesized that 1) women with PE exhibit increased plasma IL-17A and related cytokines and 2) high dietary salt intake elevates circulating IL-17A in patients with PE compared to women with healthy pregnancy (HP) and non-pregnant (NonP) women. Main outcome measures: Plasma concentration of cytokines IL-17A, IFN-γ, IL-10, TNF, IL-6, and IL-1β in samples from NonP women (n = 13), HP (n = 15), and women with PE (n = 7). Study Design: Biobanked samples from a randomized, double-blind, cross-over placebo-controlled dietary intervention study. Participants received a low sodium diet (50–60 mmol NaCl/24 h) for 10 days and were randomly assigned to ingest placebo tablets (low salt intake) or salt tablets (172 mmol NaCl/24 h, high salt intake) for 5 + 5 days. Plasma samples were drawn at baseline and after each diet. Results: While a high salt diet suppressed renin, angiotensin II, and aldosterone levels, it did not affect blood pressure or plasma cytokine concentrations in any group compared to low salt intake. Plasma TNF was significantly higher in PE than in HP and NonP at baseline and after a low salt diet. Plasma IL-6 was significantly higher in PE compared to HP at baseline and NonP at low salt. Conclusion: Interleukin-17A and related T-cell and macrophage-cytokines are not sensitive to salt-intake in PE. Preeclampsia is associated with elevated levels of TNF and IL-6 macrophage-derived cytokines. Salt-sensitive changes in systemic IL-17A are less likely to explain hypertension in PE.

OriginalsprogEngelsk
TidsskriftPregnancy Hypertension
Vol/bind35
Sider (fra-til)82-87
ISSN2210-7789
DOI
StatusUdgivet - mar. 2024

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