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Objective: This study compared the catechin composition of different tea byproducts and investigated the effects of dietary supplementation with green tea byproducts on the accumulation of abdominal fat, the modulation of lipid metabolism, and the inflammatory response in red feather native chickens. Methods: Bioactive compounds were detected, and in vitro antiobesity capacity analyzed via 3T3L1 preadipocytes. In animal experiments, 320 onedayold red feather native chickens were divided into 4 treatment groups: control, basal diet supplemented with 0.5% Jinxuan byproduct (JBP), basal diet supplemented with 1% JBP, or basal diet supplemented with 5x106 colonyforming unit (CFU)/kg Bacillus amyloliquefaciens+5x106 CFU/kg Saccharomyces cerevisiae (BA+SC). Growth performance, serum characteristics, carcass characteristics, and the mRNA expression of selected genes were measured. Results: This study compared several cultivars of tea, but Jinxuan showed the highest levels of the antiobesity compound epigallocatechin gallate. 3T3L1 preadipocytes treated with Jinxuan extract significantly reduced lipid accumulation. There were no significant differences in growth performance, serum characteristics, or carcass characteristics among the groups. However, in the 0.5% JBP group, mRNA expression of fatty acid synthase (FAS) and acetylCoA carboxylase (ACC) were significantly decreased. In the 1% JBP group, FAS, ACC and peroxisome proliferatoractivated receptor γ levels were significantly decreased. Moreover, inflammationrelated mRNA expression levels were decreased by the addition of JBP. Conclusion: JBP contained abundant catechins and related bioactive compounds, which reduced lipid accumulation in 3T3L1 preadipocytes, however there was no significant reduction in abdominal fat. This may be due to a lack of active antiobesity compounds or because the major changes in fat metabolism were not in the abdomen. Nonetheless, lipogenesisrelated and inflammationrelated mRNA expression were reduced in the 1% JBP group. In addition, dietary supplementation with tea byproducts could reduce the massive amount of byproducts created during tea production and modulate lipid metabolism and the inflammatory response in chickens. [ABSTRACT FROM AUTHOR]

. The chemokine monokine induced by interferon-γ (Mig) is involved in the recruitment of inflammatory cells and liver injury during hepatitis B virus (HBV) infection. HBV protein X contributes to Mig expression in vitro by activation of nuclear factor (NF)-κB; however, the molecular mechanisms by which HBV induces Mig expression in vivo are unknown. In this paper, we established a mouse model for HBV study by tail vein injection of HBV genome-containing adenovirus vectors. Host immune response to the secreted hepatitis B surface antigen and e antigen was detected and serum alanine aminotransferase (ALT) was elevated at different time points. We also demonstrated that peripheral and intrahepatic Mig expression was increased after Ad-HBV infection. This was followed by inflammatory cell migration and formation of inflammatory foci in the liver. In addition, NF-κB p65 subunit translocated from the cytoplasm to the nucleus, and phosphoinositide 3-kinase/Akt, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) were to some extent phosphorylated after HBV injection. Following tail vein injection of Mig siRNA/ in vivo-jetPEI-Gal complex, Mig expression was partially suppressed, inflammatory cell migration was inhibited, serum level of ALT were reduced. In conclusion, through NF-κB activation, HBV induced Mig expression in vivo, which recruited peripheral inflammatory cells to the liver and resulted in liver damage. Phosphorylation of phosphoinositide 3-kinase/Akt, ERK and JNK but not p38 might involved in the molecular mechanisms underlying HBV induced Mig expression in vivo. [ABSTRACT FROM AUTHOR]

Macrophages express a broad range of plasma membrane receptors that mediate their interactions with natural and altered-self components of the host as well as a range of microorganisms. Recognition is followed by surface changes, uptake, signaling, and altered gene expression, contributing to homeostasis, host defense, innate effector mechanisms, and the induction of acquired immunity. This review covers recent studies of selected families of structurally defined molecules, studies that have improved understanding of ligand discrimination in the absence of opsonins and differential responses by macrophages and related myeloid cells. [ABSTRACT FROM AUTHOR]

Thermal regulation of the immune response was studied in toads following single injections of bacteriophage f2. The immune response was markedly inhibited in animals kept at 15° as compared to the controls (25°). The appearance of serum antibodies was delayed in animals kept at 15° for the first post-immunization week but their peak antibody levels were similar to those in toads maintained at 25° throughout. Transfer of animals from 25° to 15° 2 weeks after immunization only temporarily depressed the serum antibody levels but caused a marked delay in conversion from heavy to light antibodies. Our results are in keeping with the hypothesis that lowered environmental temperatures inhibit a variety of metabolic processes which may be concerned with the utilization of antigen and/or the synthesis of antibodies. [ABSTRACT FROM AUTHOR]

The primary and secondary immune responses of toads (Bufo marinus) were studied using the bacteriophage f2 as antigen. Antibodies were identified in the serum 2 weeks after primary immunization and peak antibody levels were reached at 6 weeks. Although both IgM and IgG antibodies can be found in toad serum, most of the antibody activity in our animals persisted in the IgM fraction until 8 weeks after immunization. When a second injection of antigen was given 4 weeks after primary immunization, there was a marked increase in the total serum antibody activity and IgG antibodies were found as early as 4 weeks after the second injection of antigen. These observations suggest that the toad, B. marinus, is capable of a true secondary response to the bacteriophage f2. [ABSTRACT FROM AUTHOR]