High sugar intake worsens autoimmune disease in mice
More than 50 million Americans have an autoimmune disease, such as Crohn’s disease and multiple sclerosis, in which the body’s own immune system mistakenly attacks normal tissues. While the causes of such diseases are unknown, it is thought that diet may play a role. People in Western countries tend to eat diets that are high in salt, fat, and sugar. Previous studies have found that high salt intake can worsen the symptoms of many autoimmune diseases and it is possible sugar may play a role as well.
IRP researchers led by Wanjun Chen, M.D., used mice as a model system for observing the effects of high sugar consumption on autoimmune diseases. The researchers used one group of mice with symptoms similar to those of Crohn’s disease and another group with a condition resembling multiple sclerosis. The IRP team found that autoimmune symptoms worsened in both sets of mice when they were fed water mixed with a concentration of sugar similar to the amount in sweetened drinks humans often consume. In addition, the researchers discovered that high sugar intake boosts creation of highly reactive molecules called reactive oxygen species (ROS) in certain immune cells, which then triggers a signaling molecule called TGF-beta that increases production of inflammation-promoting immune cells called Th17 cells. A number of environmental pollutants, as well as drugs and tobacco, also trigger release of ROS, which is known to damage tissue when present at high levels.
This study identified a previously unrecognized mechanism by which high sugar intake stimulates Th17 cell production and worsens autoimmune symptoms in mice. The findings suggest that a low-sugar diet may help prevent or treat autoimmune diseases such as Crohn’s disease and multiple sclerosis.
Zhang D, Jin W, Wu R, Li J, Park SA, Tu E, Zanvit P, Xu J, Liu O, Cain A, Chen W. (2019). High glucose intake exacerbates autoimmunity through reactive-oxygen-species-mediated TGF-β cytokine activation. Immunity. Oct 15;51(4):671-681.e5. doi: 10.1016/j.immuni.2019.08.001.