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Immune function is altered during obesity. Moreover, males and females across different species demonstrate distinct susceptibility to several diseases. However, less is known regarding the interplay between high-fat diet (HFD) and sex in the context of immune function.The objective was to determine sex differences on immune function in response to an HFD compared with a control low-fat diet (LFD) in Wistar rats.At 5 wk of age, male and female Wistar rats were randomly assigned to 1 of 2 diets for 9 wk: ad libitum control LFD (20 kcal% fat, 53 kcal% carbohydrate, and 27 kcal% protein) or HFD (50 kcal% fat, 23 kcal% carbohydrate, and 27 kcal% protein). At 13 wk of age, rats were killed and splenocytes were isolated. Immune cell subsets were determined by flow cytometry. Immune cell function was determined by measuring the ex vivo cytokine production following stimulation with mitogens. Two-factor ANOVA was used to assess the main effect of sex, diet, and their interaction.Males gained more weight than females (410 ± 46 vs. 219 ± 45 g), independently of diet (P-sex 0.01). The HFD led to a lower production of IL-2 while increasing the production of IL-10 (both P-diet ≤ 0.05), independently of sex. HFD-fed females had increased production of cytokines (IL-2 and IL-6) after stimulation with phorbol 12-myristate 13-acetate plus ionomycin (PMA+I), as well as a higher T-helper (Th) 1:Th2 balance compared with HFD-fed males (all P 0.05). Males fed the HFD had significantly lower production of IL-2 upon stimulation compared with all other groups.Female Wistar rats developed a milder obesity phenotype and maintained enhanced cytokine production compared with males fed the HFD. Sex differences modulate immune function in the context of high-fat feeding and it should be considered in research design to establish personalized health-related recommendations.

OBJECTIVES: Studies have suggested that high-fat (HF) diets are associated with immune dysfunction, which results in a lower production of IL-2 and a lower proportion of helper T cells. Providing a diet containing 100% phosphatidylcholine (PC), a form of choline mainly found in eggs, has been shown to increase IL-2 production early in life. However, this is of no relevance for human consumption since no human diet will contain 100% PC. Therefore, the objective of this study was to determine the dose effect of egg-PC added to a high fat diet compared to a control high fat and low fat diets on T cell function in male Wistar rats. METHODS: At four weeks of age, male Wistar rats were randomized to consume one of 6 diets: 1- Control low fat (CLF, 10%wt/wt fat, 100% free choline (FC), n = 10); 2- Control high fat (CHF, 25% wt/wt fat, 100% FC, n = 10); 3- 100% PCHF (100PCHF, 25% wt/wt fat, 100% PC, n = 10); 4- 75% PCHF (75PCHF, 25% wt/wt fat, 75% PC, 25% FC, n = 10); 5- 50% PCHF (50PCHF, 25% wt/wt fat, 50% PC, 50% FC, n = 10); 6- 25% PCHF (25PCHF; 25% wt/wt fat, 25% PC, 75% FC, n = 10). Fatty acid composition was closely matched in all of the diets. Anthropometric data was collected through the duration of the study (12 weeks). At the end of the study, splenocytes phenotypes were measured by flow cytometry. RESULTS: From week 1 to week 10 there was no difference in body weight between the diets. Starting from week 2 the CLF group had a higher food intake compared to the other groups. The 50PCHF diet had a higher proportion of helper T cells (CD4+) compared to the CLF and CHF diets. In addition, 50PCHF had a higher proportion of helper T cells expressing IL-2 receptors (CD4+CD25+) compared to 25PCHF (P