Protective effects of probiotics against tannin-induced immunosuppression in broiler chickens.

Tannins (TAs) are an anti-nutritional substance commonly used as a natural feed additive for livestock. However, our previous study described the dose-dependent adverse effects of TA on immune responses and growth in chickens. In this study, we evaluated the protective effects of a probiotic preparation (BT) consisting of three different bacteria (Bacillus mesenteric, Clostridium butyricum, and Streptococcus faecalis) against TA-induced immunosuppression in chickens. Forty chicks were divided into 4 groups as follows: the CON group (basal diet), BT group supplemented with 3 g BT/kg diet, tannic acid (TA) group supplemented with 30 g TA/kg diet, and BT+TA group supplemented with 3 g BT/kg diet + 30 g TA/kg diet. The feeding trial lasted for 35 days. Lymphocyte subset, macrophage phagocytosis, cytokine mRNA expression, and primary and secondary IgY immune responses were evaluated. BT supplementation significantly improved TA-induced reductions in final body weight, body weight gain, feed intake, and relative weights of lymphoid organs compared with the TA group. Furthermore, in the spleen and cecal tonsil (CT), the relative populations of CD4+, CD8+, and CD4+CD8+ cells in the BT+TA group were significantly ameliorated compared with the TA group. Additionally, comparison with the TA group showed that the chickens in the BT+TA group had an improved relative population of B cells in the CT and that macrophage phagocytosis in the spleen was significantly increased. Chickens in the BT+TA group showed significant increases in IFN-γ and IL-4 mRNA expression in the spleen compared with the TA group. The primary and secondary IgY responses were significantly improved. These results revealed that supplementation with BT protects against TA-induced immunosuppression in chickens.

Different doses of tannin reflect a double-edged impact on broiler chicken immunity.

Tannin is one of the most common phytochemical secondary phenolic metabolites, which is widely distributed in various plant production systems. Dietary intake of tannin can exert different actions on the immune system. The aim of this study was to evaluate the influence of different concentrations on broiler chicken immunity. Three groups (n = 10 in each group) were evaluated: control group given a normal basal diet, high tannic acid (HT) group given high-dose tannic acid (30 g/kg diet) and low tannic acid (LT) group given low-dose tannic acid (0.5 g/kg diet) for 35 days. Feed intake and body weight were measured weekly. Cells were isolated from thymus, spleen and caecal tonsils at the end of the study. Lymphocyte subsets, monocytes phagocytosis and cytokine mRNA expression in spleen were evaluated. The results showed that HT group chickens had decreased daily gain, final body weight, daily feed intake and relative weights of lymphoid organs compared with other groups. In thymus, spleen and caecal tonsils, relative CD4+, CD8+, CD4+CD8+ and γδ+ cell populations in the HT group were significant decreased in comparison with those of other groups. The relative B cell population in the HT group was also significant decreased. Cytokine mRNA expression in spleen cells of the HT group was also significantly lower than that in other groups. Conversely, CD4+CD8+ subpopulations in spleen and caecal tonsils, γδ+ cells in spleen and B cells in caecal tonsils of the LT group were significantly higher than those of the control group. In addition, IFN-γ mRNA expression in the LT group was significantly higher than that of the control group. These results demonstrated that dietary intake of tannin had positive and negative effects on broiler chicken immunity in a dose-dependent manner.

Prenatal Exposure to DEHP Induces Neuronal Degeneration and Neurobehavioral Abnormalities in Adult Male Mice.

Phthalates are a family of synthetic chemicals that are used in producing a variety of consumer products. Di-(2-ethylhexyl) phthalate (DEHP) is an widely used phthalate and poses a public health concern. Prenatal exposure to DEHP has been shown to induce premature reproductive senescence in animal studies. In this study, we tested the hypothesis that prenatal exposure to DEHP impairs neurobehavior and recognition memory in her male offspring and we investigated one possible mechanism-oxidative damage in the hippocampus. Pregnant CD-1 female mice were orally administered 200 µg, 500 mg, or 750 mg/kg/day DEHP or vehicle from gestational day 11 until birth. The neurobehavioral impact of the prenatal DEHP exposure was assessed at the ages of 16-22 months. Elevated plus maze and open field tests were used to measure anxiety levels. Y-maze and novel object recognition tests were employed to measure memory function. The oxidative damage in the hippocampus was measured by the levels of oxidative DNA damage and by Spatial light interference microscopic counting of hippocampal neurons. Adult male mice that were prenatally exposed to DEHP exhibited anxious behaviors and impaired spatial and short-term recognition memory. The number of hippocampal pyramidal neurons was significantly decreased in the DEHP mice. Furthermore, DEHP mice expressed remarkably high levels of cyclooxygenase-2, 8-hydroxyguanine, and thymidine glycol in their hippocampal neurons. DEHP mice also had lower circulating testosterone concentrations and displayed a weaker immunoreactivity than the control mice to androgen receptor expression in the brain. This study found that prenatal exposure to DEHP caused elevated anxiety behavior and impaired recognition memory. These behavioral changes may originate from neurodegeneration caused by oxidative damage and inflammation in the hippocampus. Decreased circulating testosterone concentrations and decreased expression of androgen receptor in the brain also may be factors contributing to the impaired neurobehavior in the DEHP mice.