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Could Artificial Sweeteners Have a Future in Autoimmunity Treatment?

Sweetener on a metal spoon.
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Earlier this year, researchers at the Francis Crick Institute conducted a murine study indicating that sucralose, an artificial sweetener commonly found in drinks and food, may have the potential to suppress immune responses, particularly those involving T cells.


While the study was carried out on mice, it raises the possibility that similar effects might be observed in humans, leading to potential therapeutic applications for managing diseases where excessive T-cell activation is problematic, such as autoimmune conditions.

The impact of sucralose on the immune system in mice

The impact of sucralose on the human body is not fully understood. Recent research has suggested that sucralose can affect human health by influencing the microbiome. In this study, published in Nature, the researchers administered high doses of sucralose to mice at levels corresponding to the acceptable daily intake recommended by European and American food safety authorities.


The study found that mice fed high doses of sucralose showed reduced T-cell activation in response to cancer or infection. This dampening effect was specific to T cells, with no noticeable impact on other types of immune cells. Upon closer examination, the researchers discovered that high-dose sucralose affected intracellular calcium release in response to stimulation, thus impairing T-cell function.

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In mice with T cell mediated autoimmune disease, a high-dose sucralose diet helped to mitigate the harmful effects of their overactive T cells. Professor Neil Mabbott, personal chair in immunopathology at the Roslin Institute, University of Edinburgh, said: “the study also showed that the effects of high doses of sucralose on T cells delayed the development [of] the autoimmune disease type-1 diabetes. Further research on how sucralose affects T cell function may identify new methods to treat certain T cell-related autoimmune diseases such as Type 1 diabetes.”


This research should not be a cause for concern among individuals seeking to maintain a healthy immune system, as typical or moderately elevated levels of sucralose in the diet are unlikely to expose humans to the high levels used in the study. Dr. Fabio Zani, co-first author and postdoctoral fellow at the Francis Crick Institute, said: “We do not want people to take away the message that sucralose is harmful if consumed in the course of a normal balanced diet, as the doses we used in mice would be very hard to achieve without medical intervention.”

The future of sucralose as a possible therapeutic

A research highlight published in response to the Nature study set out to investigate the potential of sucralose to modulate autoimmune diseases. “Despite the experimental nature of data with limited transferability to humans due to differences in immune system function, genetic variability between the species, and high heterogeneity in genetic background and lifestyle in humans… the potential benefit of high-dose sucralose on T-cell proliferation and effector function merits further studies for conditions of uncontrolled T-cell activation in humans,” the authors write.


Dr. Karen Vousden, senior author and principal group leader at the Francis Crick Institute, said: “More research and studies are needed to see whether these effects of sucralose in mice can be reproduced in humans. If these initial findings hold up in people, they could one day offer a way to limit some of the harmful effects of autoimmune conditions.”


References:


Zani F, Blagih J, Gruber T, et al. The dietary sweetener sucralose is a negative modulator of T cell-mediated responses. Nature. 2023;615(7953):705-711. doi: 10.1038/s41586-023-05801-6


Kränkel N, Rauch-Kroehnert U. Artificial sweetener sucralose: a possible modulator of autoimmune diseases. Sig Transduct Target Ther. 2023;8(1):1-3. doi: 10.1038/s41392-023-01607-0


This article is a rework of a press release issued by the Francis Crick Institute. Material has been edited for length and content.