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Effects of altered salt intake and diet on cytokines in humans: A 20‐week randomized cross‐over intervention study

High sodium concentration alters leukocyte activation, and in particular T‐helper (Th) lymphocyte polarization, and drives the development of autoimmune diseases in mouse studies. Similar results have been obtained with human leukocytes under in vitro settings and in few observational studies. There...

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Detalles Bibliográficos
Autores principales: Niiranen, Teemu, Erlund, Iris, Jalkanen, Sirpa, Jula, Antti, Salmi, Marko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10100453/
https://www.ncbi.nlm.nih.gov/pubmed/36330564
http://dx.doi.org/10.1002/eji.202250074
Descripción
Sumario:High sodium concentration alters leukocyte activation, and in particular T‐helper (Th) lymphocyte polarization, and drives the development of autoimmune diseases in mouse studies. Similar results have been obtained with human leukocytes under in vitro settings and in few observational studies. Therefore, salt has been implicated as a risk factor for autoimmune diseases. Here, we examined whether physiologically relevant changes in salt intake or diet alter cytokine concentrations. In a 20‐wk double‐blinded, placebo‐controlled study 106 participants were randomized to Habitual and Healthy Nordic diets, and further to Usual Sodium and Reduced Sodium intake groups using a cross‐over setup. Plasma concentrations of 45 cytokines were measured at three different time‐points using a multiplex assay. Repeated analyses of covariance revealed that high salt ingestion (or changes in the diet) did not induce significant changes in any of the signature cytokines controlling Th1, Th2 or Th17 polarization. Several other pro‐inflammatory interleukins, chemokines and growth factors were also unaffected by the level of salt intake or changes in the diet. We conclude that in humans clinically relevant changes in salt intake or diet do not have reflections on the systemic concentrations of pro‐inflammatory cytokines in vivo.