Dietary changes can quickly modify the metabolism of T cells, but these effects are reversible.
Many people tend to consume energy-rich foods that are high in fats and carbohydrates as snacks or during social activities like eating out at a restaurant. Although the long-term effects of a high-calorie, low-nutrient diet on the immune system are well-documented, the short-term effects are not yet well-understood. Recently, a team of researchers conducted a study on how brief dietary changes affect the immune system. They found that at least one type of T-cell responds rapidly to these changes. The study, published in Nature Immunology, can aid researchers in monitoring early changes in the development of metabolic diseases.
“I’ve been dealing with how the diet influences our immune system,” said Francesco Siracusa, an immunologist at the University Medical Center Hamburg-Eppendorf and coauthor of the study. However, unlike many studies that look at the effects of high fat diets long-term, after health conditions develop, Siracusa and his team look at much earlier times, such as the influence of only a few days eating a high-calorie diet. “Obesity and chronic metabolic syndrome—all of that is out of the equation. We really focus on short-term dietary intervention,” he said.
The research team conducted a study to examine the effects of sudden changes in diet on animals. They fed the animals a high-fat diet with added cholesterol, but low fiber content for three days, followed by a regular rodent diet for another three days. This pattern was repeated every three days for a total of 12 days. Using gene set enrichment analysis, the researchers found that the diet switches caused alternating patterns of gene expression. Notably, the animals’ T cell receptor genes showed reduced expression when they were on the high-fat diet. The team also observed fewer T helper 17 (TH17) cells, which produce IL-17 cytokines, in the small intestine and intestinal lymphoid compartments of animals on the high-fat diet. They concluded that the animals on the high-fat diet had reduced expression of interleukin (IL)-17 related cytokine genes IL17a, Il17f, and Il22, compared to those on a regular diet for three days. “We were, to be honest, a bit surprised at first to see that within this very short period of time, adaptive immune cells reacted,” Siracusa said.
The initial results indicated that even a short-term change in diet could modify mucosal T cell responses. To investigate this further, the researchers infected mice with a pathogenic strain of Salmonella and compared the immune responses of mice with cytokines IL-17A and IL-17F deficiency (who ate a normal diet) to those of wild type animals that ate a regular diet or a feast diet. Both the feast diet eating mice and IL17A/IL17F-deficient mice showed lower weight and higher bacterial count in their intestines than the normal mice that ate a regular diet. Based on the data, it could be inferred that the feast diet lowered TH17 immune responses, as per Siracusa.
“I am not quite sure I would see it as an impairment of the immune response,” said Sammy Bedoui, an immunologist at the University of Melbourne who was not involved in the study. According to Bedoui, there could be evolutionarily beneficial reasons for these adaptations, such as limiting allergic or autoimmune reactions in response to large amounts of food. However, he thought that the feasting model captured an important and relevant aspect to omnivorous diets, and that the study offered important insights into the relationship between food consumption and immune responses.
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The team of Siracusa examined the impact of the feast diet on T cell metabolism. They discovered that this diet, which contained limited fiber, led to a decrease in the presence of short chain fatty acids, such as acetate and butyrate, in the intestines of mice. This decrease resulted in a reduction of cytokine production due to the reduced oxidative phosphorylation in T cells. However, these changes in T cell activity were reversible to some extent. After supplementing the mice with acetate and butyrate, the researchers observed an increase in the production of IL-17A and IL-17F, improved clearance of Salmonella, and an increase in the number of TH17 cells in the intestines. Additionally, they noted that the effects on T cell activity were temporary, as they could be reversed by either supplementing the mice with acetate and butyrate or returning them to a regular diet for three weeks.
“I would like to see more interrogation of that,” said Bedoui. In particular, he is interested in understanding if T cells return completely to their original states, as well as if repeated cycles of this type of feasting diet alter the system’s flexibility. That is something that interests Siracusa as well. “How long can you play this game?” he wondered.
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References:
1. Magnuson AM, et al. High-fat diet induced central adiposity (visceral fat) is associated with increased fibrosis and decreased immune cellularity of the mesenteric lymph node in mice. Eur J Nutr. 2020;59:1641-1654
2. Cavallari JF, et al. Different Th17 immunity in gut, liver, and adipose tissues during obesity: The role of diet, genetics, and microbes. Gut Microbes. 2016;7(1):82-89
3. Siracusa F, et al. Short-term dietary changes can result in mucosal and systemic immune depression. Nature Immun. 2023;24:1473-1486
