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Authoritative research clarifies the mechanism of high-salt diet injuring immune cells
Researches clarifies the mechanism of high-salt diet injuring immune cells. For many of us, adding salt to cooking is a normal thing. More and less, all according to personal taste.
In fact, we should take this issue seriously. After all, the result of heavy taste (excessive intake of salt) is not only an important risk factor for diseases such as high blood pressure, cardiovascular disease, stomach disease, and osteoporosis, but it also severely disrupts the energy balance of immune cells, making them unable to Normal work is ultimately harmful to health.
Recently, a new study published in the top global cardiovascular journal “Circulation” (IF=23.603) under the American Heart Association (AHA), from Max Delbrück, Helmholtz Federation, Germany The research team led by Professor Dominik Müller of the Molecular Medicine Center (MDC) clarified the effect of high-salt diet on the mitochondrial function of human mononuclear phagocytes through in vitro cell experiments and two independent clinical studies, and clarified the sodium ion content in the blood (serum Small changes in sodium) will inhibit the activity of mitochondria, thereby triggering adverse effects on immune cells.
It is known that high-salt diet is the main risk factor leading to mortality and morbidity. Serum sodium will rise briefly after a meal, and may accumulate in inflammation sites, affecting the differentiation and function of innate and adaptive immune cells.
As early as 2015, a study led by Müller found that elevated serum sodium will affect the activation and function of mononuclear phagocytes (MNP), which is the precursor of macrophages. Macrophages are an important component of the human immune system. They can swallow cell debris and garbage, digest pathogens, and play the role of “scavengers”.
In this new study, Müller’s team studied the changes in extracellular sodium ion concentration and how changes in the simulated circulation and tissues affect the early metabolism, transcription and functional adaptation of human and mouse mononuclear phagocytes (MNP). They observed in the laboratory the metabolism of monocytes and macrophages exposed to high concentrations of salt and found that changes occurred in only three hours: the high salt disrupted the respiratory chain and caused the cells to produce adenosine triphosphate (ATP). Significantly reduce and consume less oxygen (see figure below).
The respiratory chain is a continuous reaction system composed of a series of hydrogen transfer reactions and electron transfer reactions arranged in a certain order. It transfers the paired hydrogen atoms removed from metabolites to oxygen to produce water, and at the same time ATP is produced. The role of the respiratory chain represents the most basic function of mitochondria.
ATP is a universal fuel that powers all cells. It provides energy for the chemical work (synthesis of proteins and other molecules) required for muscle strength and metabolic regulation. ATP is produced in mitochondria through a series of complex biochemical reactions (ie, respiratory chain). High salt can specifically inhibit succinate-Q oxidoreductase (also called complex II) in the respiratory chain.
This causes the production of ATP to be affected. Subsequently, the energy-deficient monocytes mature in an abnormal manner. Their mission was originally to identify and remove pathogens in the body in order to fight infections more effectively. However, abnormal monocytes can promote inflammation and further increase the risk of cardiovascular disease and autoimmune disease.
Subsequently, the researchers conducted two independent clinical studies. In the first study, they asked 14 healthy male participants to add 6 grams of salt in addition to their daily diet for 14 days. In another single meal study, the researchers asked 20 participants to eat a vegetarian pizza with 10 grams of salt. Then they analyzed the monocytes in the participants’ blood.
The analysis results show that the inhibitory effect on mitochondria not only occurs after a long-term increase in salt intake, but also after eating a pizza. The data from the Pizza experiment shows how long this effect lasts. The researchers collected blood samples from the participants 3 hours and 8 hours after the participants had eaten Pizza. They found that this effect was almost impossible to measure in the 8-hour samples.
Müller said: “This is a good thing. If this is a long-term disturbance, we will worry that the cells will not get enough energy for a long time.”
Therefore, mitochondrial activity will not be permanently inhibited. In other words, if a person eats very salty food multiple times a day, the ongoing risk of sodium to mitochondrial function cannot be ruled out. But the researcher said that it needs to be tested in the future.
In summary, this study found that small molecules like sodium ions can very effectively inhibit an enzyme that plays a key role in the respiratory chain. When these ions flood into the mitochondria (which they do under various physiological conditions), they regulate the core components of the electron transport chain. Therefore, this seems to be a very basic regulatory mechanism in cells.
The researchers said that the next work will study whether high salt will also affect other types of cells through this mechanism, and believe that this is very likely. Because mitochondria are not only found in immune cells, in fact, they exist in every cell of the human body except red blood cells. In muscle cells, neurons, receptors, and egg cells that consume a lot of energy, they are quite numerous.
This study has not yet fully elucidated how different cell types regulate the influx of sodium into mitochondria. Nevertheless, the study confirmed that eating too much salt can affect immune cells, which may lead to inflammatory diseases of blood vessels or joints, as well as autoimmune diseases.
Nutrition experts recommend that adults consume a maximum of 5 to 6 grams per day. This calculation includes salt hidden in processed foods.
(source:internet, reference only)