High Fat Meal Increase of IL-17 is Prevented by Ingestion of Fruit Juice Drink in Healthy Overweight Subjects

Abstract

An emerging role of IL-17 in the inflammatory response associated with pathogenesis of neurodegeneration has been recently suggested. However, though diet represents a key factor in the modulation of inflammatory processes, evidence is not currently available on the nutritional regulation of IL-17 in humans. In a double blind, randomized, placebo controlled, crossover study, we investigated the effect of High Fat Meal (HFM) on IL-17 circulating levels in presence of a placebo (HFM-P) or with a Fruit Juice Drink (HFM-FJD) composed of pineapple, blackcurrant and plum in fourteen healthy overweight humans. Fasting in the morning subjects ingested a test meal providing 1344 Kcal. Ingestion of HFM-P induced an inflammatory response mediated by TNF-α (p < 0.001), IL-6 (p < 0.001) and IL-17 (p < 0.01). Plasma IL-17 concentration significantly increased at 1 h (+2.6 ± 1.1 pg/ml), remaining high at 4 h (+2.98 ± 1.2 pg/ml), 6 h (+2.38 ± 0.6 pg/ml) and 8 h (+2.8 ± 0.9 pg/ml) (ANOVA for time-course p=0.009). When the HFM was consumed in the presence of the FJD a marked inhibition of IL-17 response to the HFM was observed (ANOVA between treatment p=0.037). We provided, for the first time, evidence on the role of diet in modulating IL-17 production in healthy overweight subjects.

Fasting and meal-stimulated residual beta cell function is positively associated with serum concentrations of proinflammatory cytokines and negatively associated with anti-inflammatory and regulatory cytokines in patients with longer term type 1 diabetes

“…An acute meal-induced increase in IL-6 and TNF-α is known from previous studies with patients with the metabolic syndrome and type 2 diabetes and healthy overweight controls, but has not yet been determined in patients with type 1 diabetes [16][17][18][19]. Furthermore, no postprandial data are available for anti-inflammatory mediators, i.e.…”

“…Thus, we analysed the association between systemic anti-inflammatory, proinflammatory and regulatory cytokines, and fasting and mixed-meal-stimulated beta cell function in patients with type 1 diabetes within the first year of diagnosis and also in those with longer term diabetes with confirmed residual beta cell function. Furthermore, we investigated the influence of a high-protein liquid mixed meal test (MMT) on the systemic immune status of patients with type 1 diabetes, since the secretion of cytokines can be affected by food intake [16][17][18][19].…”

Functional Foods for Health: The Interrelated Antioxidant and Anti-Inflammatory Role of Fruits, Vegetables, Herbs, Spices and Cocoa in Humans

“…Dietary interventions were grouped according to different categories, specifically vegetables (Table 1 ) [26-31], fruits (Table 2 ) [32-54], grape seeds (Table 3 ) [55-59], herbs (Table 4 ) [60-65], green tea (Table 5 ) [66-70], spices (Table 6 ) [71-78], beverages with mixed composition (Table 7 ) [8, 79-82] extracts with mixed composition (Table 8 ) [83-93] and cocoa products (Table 9 ) [66, 94-97]. Selection of the plant foods was performed on the basis of available human data on both oxidative and inflammatory markers: for example, raspberry, blackberry and olives were not included due to the lack of combined information.…”

“…Increase in postprandial lipopolysaccharide (LPS) and Toll-like receptor-4 (TLR4) is associated with increased levels of inflammatory cytokines, such as interleukin (IL)-6, IL-17 and tumor necrosis factor-alpha (TNF-α) [8], which in turn activate oxidative burst [9]. Given these premises, the importance of the diet, as inducer or preventer of inflammatory and oxidative stress, is paramount.…”

Oxidative Stress in Atherosclerosis Development: The Central Role of LDL and Oxidative Burst

“…1). During the post-prandial phase, dietary fats also promote the secretion of inflammatory cytokines such as the Th1 Tumor Necrosis Factor (TNF)- [18][19][20] and the InterLeukin (IL)-17 [20]. This evidence suggests a link between post-prandial lipemia and the trigger of Th17, considering that LPS-(TLR4 ligand)-activated dendritic cells significantly increase Th17 triggering [21].…”