High-Salt Diet Inhibits Body's Ability to Fight Certain Bacterial Infections, Study Finds
Too much salt is broadly considered bad for the body, though some studies have suggested it can aid the immune system’s response to infection. New research contradicts that notion.
Eating a high-salt diet can negatively impact the body’s ability to fight off certain bacterial infections, according to new research.
The findings, published in Science Translational Medicine, are the latest evidence against eating diets rich in sodium. However, they also stand in contrast to other research, which has suggested that in some contexts salt can aid the immune system’s response to infection.
“A high-salt diet (HSD) can stimulate immunity through the nuclear factor of activated T cells 5 (Nfat5)—signaling pathway, especially in the skin, where sodium is stored. The kidney medulla also accumulates sodium to build an osmotic gradient for water conservation,” write corresponding author Christian Kurts, of the Institute for Experimental Immunology, at the University Hospital of Bonn, in Germany, and colleagues.
Kurts and his team decided to see what impact salt might have on the most common type of kidney infection, uropathogenic E coli-induced pyelonephritis. To study the question, they put mice on HSDs, and studied how the diet impacted their ability to fight off E coli kidney infections, as well as systemic infections caused by the foodborne pathogen Listeria monocytogenes. In both cases, the investigators found adding extra salt harmed the mice’s ability to fight off the infection.
In the case of pyelonephritis, salt appeared to worsen outcomes via 2 mechanisms.
“First, on an HSD, sodium must be excreted; therefore, the kidney used urea instead to build the osmotic gradient,” Kurts and colleagues write. “However, in contrast to sodium, urea suppressed the antibacterial functionality of neutrophils, the principal immune effectors against pyelonephritis.”
Secondly, Kurts and colleagues noted that the body also responds to the need to excrete sodium by suppressing aldosterone synthase. However, doing so caused an accumulation of aldosterone precursors with glucocorticoid functionality, “which abolished the diurnal adrenocorticotropic hormone—driven glucocorticoid rhythm and compromised neutrophil development and antibacterial functionality systemically.”
Glucocorticoids also played a role in the way the mice responded to Listeria monocytogenes infection, the study found.
“Glucocorticoids directly induced Nfat5 expression, but pharmacological normalization of renal Nfat5 expression failed to restore the antibacterial defense,” Kurts and colleagues write.
After their findings in mice, the team recruited 10 human volunteers and gave them a diet with extra sodium (roughly equivalent to eating 2 large fast-food meals per day). After one week on the diet, the team found that neutrophils from these human volunteers were less effective at digesting bacteria.
Though studies on patients with actual infections would be necessary to prove a connection, Kurts told Contagion® that the data suggest if a patient suffers an infection while already consuming a diet rich in sodium, cutting excess salt intake will likely benefit the patient.
“[C]hanging to a normal salt diet will likely reverse the changes of an HSD within a few days, because new neutrophils are produced every day,” he said.
Unfortunately, while ending an HSD appears to nullify negative impacts of too much salt, that does not mean a low-salt diet itself leads to an increased immune response, Kurts said, at least not in the case of pyelonephritis.
“Probably because the immunosuppressive mediator induced by salt, the glucocorticoids does not decrease below a certain baseline because they are maintained by the pituitary gland,” he said.