Prebiotics constitute emerging tools to alleviate immune pathologies. This study aimed to evaluate the effect of prebiotic exposure during perinatal and postweaning periods on immune and gut regulations. Mice were fed either a galactooligosaccharides/inulin prebiotic mix-enriched diet or a control diet during the perinatal and/or postweaning periods. Biomarkers related to gut barrier function (SCFA, heat shock proteins, zonula occludens protein-1, and mucin-2) and immune mechanisms (IgA, IgE, IgG1, IgG2a, IL-10, TGF-β, IL-4, IL-17A, and IFN-γ) were analyzed. The milk of dams fed the prebiotic diet was more concentrated in both IgA and TGF-β when prebiotics were introduced during both the perinatal and postweaning periods; IL-10, IgA, and IgG2a were increased in pups; and expression of intestinal markers was more pronounced. Postweaning exposure to prebiotics alone induced higher INF-γ and TGF-β levels, whereas IgA levels fell. Combined exposure periods (perinatal/postweaning) to prebiotics increased tolerance-related immunoglobulins in pups and reinforced gut barrier functions.

Food allergies are increasing, and no treatment exists, thus enhancing interest in prebiotic strategies. This study aimed to analyze the preventive effects of prebiotic feeding during perinatal and postweaning periods in a mouse model of allergy by studying biomarkers related to tolerance (IgG2a, IgA, IFN-γ, TGF-β, and IL-10), to allergy (IgE, IgG1, IL-4, IL-17, symptoms), and to microbiota (propionate and MyD88). Balb/c mice, both dams and their pups, were fed a diet supplemented with (+Prb) or without (-Prb) GOS/inulin prebiotics. Mice were then sensitized with allergens. Regardless of diet, sensitized mice exhibited similar levels of IgE, IgG1, CD-23, IL-4, IL-17, and symptoms. However, in comparison to -Prb-sensitized mice, +Prb-sensitized mice displayed higher concentrations of total IgG2a (6669 ± 1788 vs 3696 ± 1326 fluorescence units, p < 0.005), specific IgA (285 ± 26 vs 156 ± 9 fluorescence units, p < 0.01), IFN-γ (3194 ± 424 vs 1853 ± 434 pg/mL, p < 0.01), IL-10 (777 ± 87 vs 95 ± 136 pg/mL, p < 0.005), TGF-β (4853 ± 1959 vs 243 ± 444 pg/mL, p < 0.01), MyD88 (0.033 ± 0.019 vs 0.009 ± 0.004 relative expression, p < 0.01), and propionate (4.15 ± 0.8 vs 2.9 ± 1.15 μmol, p < 0.05). In a mouse model of allergy, prebiotic exposure during perinatal and postweaning periods induced the highest expression of biomarkers related to tolerance without affecting biomarkers related to allergy.

Hemin is a heme oxygenase-1 (HO-1) inducer which provides endogenous carbon monoxide known for playing roles in cell proliferation, inflammation or aggregation process. The objective of the current study was to examine the effect of prophylactic treatment with hemin in a thrombosis vascular model. Three groups of Wistar rats, control (n = 6), hemin (n = 6) and hemin + HO-1 inhibitor (n = 6), were used for this study. Hemin-treated animals received hemin (50 mg/kg/d; I.P.) for seven days and HO-1 inhibitor group received hemin at the same dose and SnPP IX (60 mg/kg/d; I.P.). All animals were exposed to electric stimulation of the left carotid according to Kawasaki's procedure to induce reproducible thrombus formation. The hemin treatment did not induce blood pressure disturbance. Effects of hemin on vascular thrombosis were quantified by histopathology and its influence on haemostasis was assessed by measuring prothrombin time (PT), activated partial thromboplastin time (APTT) and blood parameters at the end of treatment. The HO-1 mRNA and protein level variation were also checked out. Results showed that chronic treatment with hemin significantly (p < 0.01) reduced the vascular occlusion degree when compared to control and hemin SnPP groups with 7.2 +/- 4.6 vs. 71.1 +/- 14.7 and 74.0 +/- 8.8%, respectively. Moreover, we observed significant (p < 0.05) perturbations of blood parameters in hemin-treated and hemin-SnPP treated rats. Interestingly, hemin treatment did not significantly increase both PT and APTT. Finally, the HO-1 mRNA and protein levels were increased in hemin-treated carotid artery. In conclusion, hemin by inducing HO-1 expression may be a preventive agent against clinical disorders associated to an increased risk of thrombosis events and may limit haemorrhagic risks.

To assess the impact of prebiotic supplementation during gestation and fetal and early neonatal life, gestating BALB/cj dam mice were fed either a control or a prebiotic (galacto-oligosaccharides -inulin, 9:1 ratio)-enriched diet throughout pregnancy and lactation, and allowed to nurse their pups until weaning. At the time of weaning, male offspring mice were separated from their mothers, weaned to the same solid diet as their dam and their growth was monitored until killed 48 d after weaning. Prebiotic treatment affected neither the body-weight gain nor the food intake of pregnant mice. In contrast, at the time of weaning, pups that had been nursed by prebiotic-fed dams had a higher body weight (11·0 (SE 1·2) g) than pups born from control dams (9·8 (SE 0·9) g). At 48 d after weaning, significantly higher values were observed for colon length and muscle mass in the offspring of prebiotic-fed dams (1·2 (SE 0·1) cm/cm and 5·7 (SE 1·8) mg/g, respectively), compared with control offspring (1·1 (SE 0·1) cm/cm and 2·9 (SE 0·9) mg/g, respectively), without any difference in spleen and stomach weight, or serum leptin concentration. The present preliminary study suggests that altering the fibre content of the maternal diet during both pregnancy and lactation enhances offspring growth, through an effect on intestinal and muscle mass rather than fat mass accretion.Key words: Prebiotics: Gestation: Development: NeonatesThe prevalence of the metabolic syndrome, as defined by the combination of abdominal obesity, impaired glucose tolerance, dyslipidaemia and hypertension (1) , is increasing throughout the world. This syndrome is associated with an increased risk of CVD and type 2 diabetes (1) . The pathophysiology of the metabolic syndrome is clearly multifactorial, and besides the direct impact of dietary imbalance, there is considerable evidence that adverse environmental influences during early development may increase disease risk in later life (2) . A prebiotic is a non-viable food component that confers a health benefit on the host associated with modulation of the microbiota (3) . Prebiotic consumption may be associated with various health benefits including a reduction of colorectal cancer risk (4) , a reduction of atopic dermatitis incidence in formulafed, high-risk infants (5) and the prevention of type 2 diabetes (6) . Several studies (7,8) have described the effect of prebiotic supplementation on body weight and fat mass in adult experimental animal models. In some studies (9) , the decrease in overall fat mass, and in the various deposits of white adipose tissue, is not associated with any effect on body weight. A recent study has shown that supplementation with a mix of inulin and fructo-oligosaccharides had a significant benefit on the maintenance of an appropriate BMI and fat mass accretion in non-obese adolescents (10) .However, very little is known about the effects of consuming a high-fibre diet during pregnancy and the development of the offspring (11) . Methods Experimental procedureThe experimen...