Salt in the sights
An important factor that can cause this balance to tip over may have been identified by scientists in the US and Germany: too much salt in food. The suspicion arose, says the team around Markus Kleinewietfeld of Yale University, when an observation was made in fast food restaurants: After consuming the food there, which is notoriously over-salted, the number of certain white blood cells in the body decreased Test subjects drastically too. These were so-called T-cells, a variety that promotes inflammation.
The team now extensively studied this relationship in the laboratory, on various cultured cells and in mice. They came across a subgroup of T cells, called Th17 for short. They are among the T-helper cells that rush to the rescue of signals from other immune cells and support their colleagues in the fight against pathogens. They reside mainly in the intestine, but also in other tissues of the body. However, especially the Th17 cells have a different face too: If there are too many of them or if they develop a particularly aggressive nature, they can become traitors and attack the body's own tissue. Their involvement in, for example, multiple sclerosis, in which the immune system attacks the isolation layer around nerve cells, and psoriasis, where skin cells are the targets, has already been demonstrated in several studies. display
More and more aggressive
This malignant side of the Th17 cells apparently can be promoted by salt, the new results show. For example, when researchers increased the salt content in their petri dishes, they suddenly developed many more Th17 cells than before. This increase was sometimes very dramatic: "It can be up to ten times higher than under normal conditions, " says Kleinewietfeld. In addition, the profile of messengers that sent out and responded to these cells was slightly altered - a particularly aggressive strain had emerged.
A similar picture emerged when the scientists mixed mice with more salt in the feed than normal: as a result, their brain inflammation worsened in a similar way to that of multiple sclerosis in humans. And even with them, the number and aggressiveness of Th17 cells increased. One of the key mediators of these changes was evidently an enzyme that had previously been linked to the metabolism of the salt - not in immune cells, but in the gut and kidneys, where it coordinates the uptake of salt into the cells. If the researchers blocked this enzyme or immobilized its gene, the connection between salt concentration and immune activity disappeared.
Worked with completely wrong concentrations
The teams also identified other factors that influence the process - and they already have an idea why the context has been overlooked for so long. Normally, experiments would always be conducted in a saline-equivalent environment, explains David Hafler, senior author of the paper and also from Yale University. In the tissue, where most of the immune reactions take place, there were some completely different, significantly higher concentrations.
As logical as the context may seem, and as well as it fits the development of salinity in food and autoimmune diseases in recent decades, the interpretation of the results should be cautious, emphasize both teams. So far, they have observed the effect only in artificial systems, ie in isolated cells and in a model for a human disease. Whether there is such a connection in man, must first be shown. They now want to start clinical trials as soon as possible. And even if the suspicion is confirmed, it will almost certainly not be enough to do without salt in order to avoid the occurrence of such diseases. The salt only seems to work if it has already been a predisposition or a sensitization of the immune system. Nevertheless, it can not hurt to shut down your salt intake and this is especially true for people who suffer from this condition.Markus Kleinewietfeld (Yale University, New Haven) et al .: Nature, doi: 10.1038 / nature11868 Chuan Wu (Brigham and Women's Hospital, Harvard Medical School) et al .: Nature, doi: 10.1038 / nature11984 wissenschaft.de Ilka Lehnen-Beyel