BackgroundThe present study was conducted to investigate the effects of dietary plant-derived phytonutrients, carvacrol, cinnamaldehyde and Capsicum oleoresin, on the translational regulation of genes associated with immunology, physiology and metabolism using high-throughput microarray analysis and in vivo disease challenge model of avian coccidiosis.MethodsIn this study, we used nutrigenomics technology to investigate the molecular and genetic mechanisms of dietary modulation of host innate immunity and metabolism by three phytonutrients. To validate their immunomodulatory effects in a disease model, young broiler chickens fed a standard diet supplemented with three phytochemicals (carvacrol, cinnamaldehyde, and Capsicum oleoresin) from one day post-hatch were orally challenged with E. acervulina. The body weight gain and fecal oocyst production were used to evaluate coccidiosis disease parameters.ResultsAnalysis of global gene expression profiles of intestinal tissues from phytonutrient-fed birds indicated that Capsicum oleoresin induced the most gene changes compared to the control group where many of these genes were associated with those of metabolism and immunity. The most reliable network induced by dietary cinnamaldehyde treatment was related with the functions of antigen presentation, humoral immune response, and inflammatory disease. Furthermore, dietary supplementation with these phytonutrients significantly protected broiler chickens against live coccidiosis challenge infection based on body weight and parasite fecundity.ConclusionsThe results of this study provide clear evidence to support the idea that plant-derived phytochemicals possess immune-enhancing properties in chickens and these new findings create a new possibility to develop effective drug-free alternative strategies for disease control for poultry infectious diseases.

Objective. To investigate whether TRAIL influences the pathogenesis of osteoarthritis (OA).Methods. A recombinant adenoviral vector system (Ad- Conclusion. TRAIL induces chondrocyte apoptosis, and TRAIL-induced chondrocyte apoptosis may play a role in the pathogenesis of OA.TRAIL

Necrotic enteritis (NE) has reemerged as a significant problem as a result of growing restrictions of antibiotics in agricultural animal production and increasing concerns over antibiotic resistance in human pathogens. To enhance our understanding of host-pathogen immunobiology in NE, transcriptional analysis was conducted to compare changes in NE-induced intestinal transcripts and to identify immune-related genes whose expression are associated with NE disease resistance using two genetically disparate Fayoumi chicken lines, M5.1 and M15.2. NE was induced by co-infection of Eimeria maxima and Clostridium perfringens using an established disease model and two major NE-induced clinical signs, body weight loss and intestinal lesions, were measured in two inbred Fayoumi chicken lines, M5.1 and M15.2. In the clinical criteria, line M5.1 chickens were more resistant to NE compared to line 15.2 birds. Although they have the same genetic background, these two chicken lines are genetically disparate at their major histocompatibility complex (MHC) and this difference was reflected in the differential expression patterns of several inflammatory genes such as suppressor of cytokine signaling 3 (SOCS3), interleukin 8 (IL8), nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, zeta (NFKBIZ), serpin peptidase inhibitor, clade F (alpha-2 antiplasmin, pigment epithelium derived factor), member 1 (SERPINF1), and gap junction protein, alpha 1, 43kDa (GJA1) between NE-afflicted and uninfected chickens. These results will lead to increased insights on the NE disease resistance mechanisms and the role of host genes controlling host immune response to C. perfringens.