Friday, 18 March 2016

Is the salt story to be taken with a pinch?

Jörg S, Kissel J, Manzel A, Kleinewietfeld M, Haghikia A, Gold R, Müller DN, Linker RA. High salt drives Th17 responses in experimental autoimmune encephalomyelitis without impacting myeloid dendritic cells.Exp Neurol. 2016 Mar 11. pii: S0014-4886(16)30053-X.

Recently, we have shown that high dietary salt intake aggravates T helper cell (Th) 17 responses and neuroinflammation. Here, we employed in vitro assays for myeloid dendritic cell (mDC) maturation, DC cytokine production, T cell activation and ex vivo analyses in murine experimental autoimmune encephalomyelitis (EAE) to investigate whether the salt effect on Th17 cells is further mediated through DCs in vivo. In cell culture, an excess of 40mM sodium chloride did neither affect the generation, maturation nor the function of DCs, but, in different assays, significantly increased Th17 differentiation. During the initiation phase of MOG35-55 EAE, we did not observe altered DC frequencies or co-stimulatory capacities in lymphoid organs, while IL-17A production and Th17 cells in the spleen were significantly increased. Complementary ex vivo analyses of the spinal cord during the effector phase of EAE showed increased frequencies of Th17 cells, but did not reveal differences in phenotypes of CNS invading DCs. Finally, adaption of transgenic mice harboring a MOG specific T cell receptor to a high-salt diet led to aggravated clinical disease only after active immunization. Wild-type mice adapted to a high-salt diet in the effector phase of EAE, bypassing the priming phase of T cells, only displayed mildly aggravated disease. In summary, our data argue for a direct effect of NaCl on Th17 cells in neuroinflammation rather than an effect primarily exerted via DCs. These data may further fuel our understanding on the dietary impact on different immune cell subsets in autoimmune diseases, such as multiple sclerosis.

As we have been following the salt story (based on altmetrics one of the MS stories of the decade:-) you may be interested in this, so eating the equivalent of half a kilo of salt a day makes you get worse EAE in some strains and sex by promoting Th17 cells.

In this study it doesn't affect dendritic cells so it may be working on
the T cells directly. So they got more severe EAE with salt and if
you have more severe EAE you have more cells in the spinal cord as they are causally linked but it is Th17 rather than Th1 that go in

However if after the disease induction then it didn't do much implying the major effect is acting on whether one becomes sensitized rather than having an effect once you are sensitized meaning there is less impact on the condition after it has started.
This what was originally thought

Any way before you change your life style back to salt, make sure your kids don't eat too much salt. Also please remember folks don't eat half a kilo of salt a day, not because it would make your MS worse, but because it will kill you. 

However please do watch your salt intake as we know, too much of a good thing is not good for you.


  1. I don't think salt recommendations should be given based on some mice experiments.

  2. Forgive my ignorance, by why would the researchers use such a high amount of salt in their study? Wouldn't it make sense to use the RDA dose equivalent?

    1. I suspect it won't do anything and then the story would fall apart to a nothing story?

      But this is the problem of rubbish refereeing, if the isue of a dose response was asked for in the fist instance this would be known but this was a case of doing experiments to prove the news story

  3. I have been reading that sea salt is far healthier than table salt. And that sea salt will not raise blood pressure but table salt will? Is this correct?
    I wonder if sea salt is different to table salt in it's impact on EAE and MS?

    1. I suspect this is not correctbut I dont knowfor definite


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