Eating
too much salt, which is common in many Western societies, is not only
bad for our blood pressure and cardiovascular system – it could also
adversely impact the immune system. An international research team, is
now reporting in “Cell Metabolism” that salt can disrupt key immune
regulators called regulatory T cells by impairing their energy
metabolism. The findings may provide new avenues for exploring the
development of autoimmune and cardiovascular diseases.
A
few years ago, research by teams revealed that too much salt in our
diet can negatively affect the metabolism and energy balance in certain
types of innate immune cells called monocytes and macrophages and stop
them from working properly. They further showed that salt triggers
malfunctions in the mitochondria, the power plants of our cells.
Inspired by these findings, the research groups wondered whether
excessive salt intake might also create a similar problem in adaptive
immune cells like regulatory T cells.
Regulatory
T cells, also known as Tregs, are an essential part of the adaptive
immune system. They are responsible for maintaining the balance between
normal function and unwanted excessive inflammation. Tregs are sometimes
referred to as the “immune police” because they keep bad guys like
autoreactive immune cells at bay and ensure that immune responses happen
in a controlled way without harming the host organism.
Scientists
believe that the deregulation of Tregs is linked to the development of
autoimmune diseases like multiple sclerosis. Recent research has
identified problems in mitochondrial function of Tregs from patients
with autoimmunity, yet the contributing factors remain elusive.
“Considering our previous findings of
salt affecting mitochondrial function of monocytes and macrophages as
well as the new observations on mitochondria in Tregs from autoimmune
patients, we were wondering if sodium might elicit similar issues in
Tregs of healthy volunteers,” says the senior author.
Previous
research has also shown that excess salt could impact Treg function by
inducing an autoimmune-like phenotype. In other words, too much salt
makes the Treg cells look like those involved in autoimmune conditions.
However, exactly how sodium impairs Treg function had not yet been
uncovered.
The
new international study has now discovered that sodium disrupts Treg
function by altering cellular metabolism through interference with
mitochondrial energy generation. This mitochondrial problem seems to be
the initial step in how salt modifies Treg function, leading to changes
in gene expression that showed similarities to those of dysfunctional
Tregs in autoimmune conditions.
Even
a short-term disruption of mitochondrial function had long-lasting
consequences for the fitness and immune-regulating capacity of Tregs in
various experimental models. The new findings suggest that sodium may be
a factor that could contribute to Treg dysfunction, potentially playing
a role in different diseases, although this needs to be confirmed in
further studies.
“The
better understanding of factors and underlying molecular mechanisms
contributing to Treg dysfunction in autoimmunity is an important
question in the field. Since Tregs also play a role in diseases such as
cancer or cardiovascular disease, the further exploration of such
sodium-elicited effects may offer novel strategies for altering Treg
function in different types of diseases,” says another author. “However,
future studies are needed to understand the molecular mechanisms in
more detail and to clarify their potential relationship to disease.”
https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00009-8
http://sciencemission.com/site/index.php?page=news&type=view&id=publications%2Fsodium-perturbs&filter=22