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Context Ocimum sanctum Linn (Labiatae) (OS), Zingiber officinale Rose (Zingiberaceae) (ZO), and Piper nigrum Linn (Piperaceae) (PN) are used in traditional medicine as immunomodulator, anti-inflammatory, and bioavailability enhancer agents. Objective Active phytoconstituents of OS, ZO, PN hydro-alcoholic extracts and their effects on gut microbiota, basal inflammation and lipid profile were investigated in rats. Materials and methods Active phytoconstituents of extracts were analysed using HPLC and GC-MS. SD rats were supplemented with individual/combined extracts (OS-850; ZO-500; PN-100 mg/kg Bw) and Fructooligosaccharide (standard prebiotic-5g/kg-Bw), orally for 30 days. Haematology, lipid profile, LPS, CRP, IL-6, insulin and histology of vital organs were analysed. Caecal bacterial levels were assessed by RT-PCR. Results High content of phenolic compounds luteolin-7- O -glucoside (430 ± 2.3 mg/100g), gallic acid (84.13 ± 1.2 mg/100 g) and flavones (88.18 ± 1.8 mg/100 g) were found in OS, ZO, and PN, respectively. Combined extract was rich in luteolin-7- O -glucoside (266.0 ± 1.80 mg/100 g). Essential oils including methyleugenol (13.96%), 6-shogaol (11.00%), piperine (18.26%), and cyclopentasiloxane (10.06%) were higher in OS, ZO, PN and combined extract. Higher levels of caecal Lactobacillus (1.7–3.4-fold), Bifidobacterium (5.89-28.4-fold), and lower levels of Firmicutes (0.04–0.91-fold), Bacteroides (0.69–0.88-fold) were noted among extracts and FOS supplemented rats. Significant ( p < 0.05) decrease in plasma lipid profile and LPS was noted in all supplemented rats. Discussion and conclusions The current study could be first of its kind in exploring prebiotic potential of OS, ZO, PN and their effect on native gut bacterial population.

Synbiotic supplementation to pregnant dams affected the offspring's cellular and mucosal immunity favorably. However, IgG response to Hepatitis-B vaccine was influenced positively only when the supplementation was extended to the offsprings in the post weaning period. © 2016 Society of Chemical Industry.

The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\Fe-deficient weanling SD rats. Rats were fed a control (CD) or Fe-deficient (ID) diet for 4 weeks and then evaluated for hemoglobin (Hb) and serum Fe status. Then, half the rats in each group began to receive daily oral Pb exposure (25 mg/4 ml/kg BW; gavage) or vehicle for a further 4 weeks (while maintained on original respective diets). After the 4-weeks of dosing, rats were assessed for Hb and serum Fe, and for blood lead level (BLL) and d-aminolevulinic acid dehydratase (ALAD) activity. At this point, half the rats in each group (now n ¼ 8) were then vaccinated with tetanus toxoid (TT), and then two boosters at 2-week intervals. All the time, rats stayed on their original respective diets along with exposure to Pb on alternate days. At 2 weeks after the final booster, rats were euthanized and blood collected to assess total/specific IgG and IgM levels; mucosal (intestinal) IgA levels were also determined. Spleens were taken to assess CD4 þ and CD8 þ cell levels and for ex vivo measures of splenocyte proliferation/T H 1 and T H 2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4 þ cell levels were not impacted by treatment; CD8 þ levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes.

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