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Alto teor de sal da dieta piora doenças autoimunes


Créditos: Fotógrafo Marcos Santos / USP Imagens

Várias evidências científicas mais recentes dão conta do sal como indutor de autoimunidade, em mecanismos não plenamente reconhecidos. No dia de hoje vemos a publicação da relação entre o consumo excessivo de sal e a atividade da esclerose múltipla, com a hipótese de ativação dos macrófagos como mecanismo fisiopatogênico.

J Autoimmun. 2015 Nov 13. pii: S0896-8411(15)30052-4. doi: 10.1016/j.jaut.2015.11.001. [Epub ahead of print]
Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity.
Hucke S1, Eschborn M1, Liebmann M1, Herold M1, Freise N2, Engbers A1, Ehling P1, Meuth SG3, Roth J2, Kuhlmann T4, Wiendl H3, Klotz L5.
The increasing incidence in Multiple Sclerosis (MS) during the last decades in industrialized countries might be linked to a change in dietary habits. Nowadays, enhanced salt content is an important characteristic of Western diet and increased dietary salt (NaCl) intake promotes pathogenic T cell responses contributing to central nervous system (CNS) autoimmunity. Given the importance of macrophage responses for CNS disease propagation, we addressed the influence of salt consumption on macrophage responses in CNS autoimmunity. We observed that EAE-diseased mice receiving a NaCl-high diet showed strongly enhanced macrophage infiltration and activation within the CNS accompanied by disease aggravation during the effector phase of EAE. NaCl treatment of macrophages elicited a strong pro-inflammatory phenotype characterized by enhanced pro-inflammatory cytokine production, increased expression of immune-stimulatory molecules, and an antigen-independent boost of T cell proliferation. This NaCl-induced pro-inflammatory macrophage phenotype was accompanied by increased activation of NF-kB and MAPK signaling pathways. The pathogenic relevance of NaCl-conditioned macrophages is illustrated by the finding that transfer into EAE-diseased animals resulted in significant disease aggravation compared to untreated macrophages. Importantly, also in human monocytes, NaCl promoted a pro-inflammatory phenotype that enhanced human T cell proliferation. Taken together, high dietary salt intake promotes pro-inflammatory macrophages that aggravate CNS autoimmunity. Together with other studies, these results underline the need to further determine the relevance of increased dietary salt intake for MS disease severity.