Expression of TGF-ß/Smads in Cecum and Spleen of Chicken Infected with E. Tenella

Chicken coccidiosis is a common and severe parasitic disease caused by infection from Eimeria spp., which affects the integrity of the intestinal mucosa. TGF-ß has been shown to play an important role in the healing of intestinal mucosas, immunity, and the maintenance of bowel mucosa integrity. Very little is known about the presence of the components of TGF-ß/Smads signaling pathway of chicken at different times following coccidian infection. In the present study, we measured the levels of TGF-ß2, 3, 4, receptor TßRI, II, down-stream Smad 2, 3, 7 in cecum and spleen of chicken at different times after inoculation with Eimeria tenella using quantitative real-time PCR. The results showed that the TGF-ß/Smads signaling pathway was not activated in cecum in the early stage of infection. However, on the 8th day, the expression of TGF-ß2, 4, down-stream protein Smad 2, 7 were significant up-regulated in the spleen, which indicated that the TGF-ß/Smads signaling was changed in the E. tenella infection and was differentially expressed in various tissues in the early stages of infection.(AU)

Suppresses of Astragalus Polysaccharide on E. coli-Induced Injured Intestinal Microvascular through TLR4-NF-B Signal Pathways in Chickens

To investigate the hypothesis that APS can attenuate E. coli-induced microvascular dysfunction in chicken intestine, 60 0-day old male chickens were divided into three groups with 5 replications of 4 chicks. Chicken in the APS group were treated with 15 mg APS daily while the others were given 0 mg APS for 6 days. Then all 7-day old chicken were injected intraperitoneally by E. coli, except for the chicken in the control group. After 4 h, all chickens intestinal samples were collected to detect gene expressions involved in inflammatory factors and adhesion molecules. Results showed that APS attenuated the signs of edema and hemorrhage in 7-day old chicken intestinal mucosa which were induced by E. coli injection. Consistently, APS significantly reduced the increasing mRNA levels of inflammatory factors such as Tumor necrosis factor-a (TNF-a), interleukin (IL) -1 and inducible nitric oxide synthase (iNOS) (p 0.05), the same results were observed in vascular adhesion molecules such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, we observed that APS supplementation in water suppressed significantly (p 0.05) the decline of reparative factors such as epithelial growth factor (EGF) and basic fibroblast growth factor (bFGF) in E. coli injected group. Furthermore, supplementation with APS substantially blocked (p 0.05) the increase in Toll-like receptor-4 (TLR4) and Nuclear factor (NF)-B mRNA abundance (p=0.087) induced by E. coli infection. This study indicated that microvascular injured chicken intestine induced by E. coli would be attenuated with feeding APS, and the mechanism of repairing were probably mediated through TLR4-NF-B signal pathways.(AU)

Suppresses of Astragalus Polysaccharide on E. coli-Induced Injured Intestinal Microvascular through TLR4-NF-B Signal Pathways in Chickens

To investigate the hypothesis that APS can attenuate E. coli-induced microvascular dysfunction in chicken intestine, 60 0-day old male chickens were divided into three groups with 5 replications of 4 chicks. Chicken in the APS group were treated with 15 mg APS daily while the others were given 0 mg APS for 6 days. Then all 7-day old chicken were injected intraperitoneally by E. coli, except for the chicken in the control group. After 4 h, all chickens intestinal samples were collected to detect gene expressions involved in inflammatory factors and adhesion molecules. Results showed that APS attenuated the signs of edema and hemorrhage in 7-day old chicken intestinal mucosa which were induced by E. coli injection. Consistently, APS significantly reduced the increasing mRNA levels of inflammatory factors such as Tumor necrosis factor-a (TNF-a), interleukin (IL) -1 and inducible nitric oxide synthase (iNOS) (p 0.05), the same results were observed in vascular adhesion molecules such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, we observed that APS supplementation in water suppressed significantly (p 0.05) the decline of reparative factors such as epithelial growth factor (EGF) and basic fibroblast growth factor (bFGF) in E. coli injected group. Furthermore, supplementation with APS substantially blocked (p 0.05) the increase in Toll-like receptor-4 (TLR4) and Nuclear factor (NF)-B mRNA abundance (p=0.087) induced by E. coli infection. This study indicated that microvascular injured chicken intestine induced by E. coli would be attenuated with feeding APS, and the mechanism of repairing were probably mediated through TLR4-NF-B signal pathways.

Resveratrol attenuates LPS-induced apoptosis via inhibiting NF-kB activity in chicken peripheral lymphocyte cultures

This study aims to investigate whether resveratrol (RES) could inhibit NF-κB activity and protect in vitro cultured chicken lymphocytes from apoptosis induced by continuous LPS stimulation. Blood lymphocytes of chickens were collected and cultured. LPS was added to the samples of treatment group, while the same volume of normal saline (NS) was supplemented to those of the control group. In the treatment groups, four different concentrations of RES (0, 20, 40, and 80 µg/ml) were admixed. Then, the following indicators were tested: lymphocyte apoptotic rate, lymphocyte viability, NF-κB activity, TNF-a level, reactive oxygen species (ROS), and expression of apoptosis-related proteins (Fas/FasL and Caspase-8). The results indicated that the application of different concentrations of RES could significantly increase the viability of lymphocytes and decrease the apoptotic rate (p<0.05) after continuous stimulations by LPS. The activity of NF-κB levels of TNF-a and ROS in the RES treatment subgroups was significantly decreased in comparison with that in the RES-blank subgroup (p<0.05). The cells in the treatment group that had been treated with 20, 40 and 80 μl/ml of RES exhibited a significantly lower Fas and Caspase-8 expression level than that in the RES-blank subgroup (p<0.05). These findings revealed that RES could substantially diminish the concentrations of ROS and TNF-a, down-regulate NF-κB activity, decrease the expression of Fas and Caspase-8, stimulate the activity of peripheral lymphocytes, and lower the rate of their apoptosis, induced by continuous LPS stimulation in chicken lymphocyte cultures.(AU)

Resveratrol attenuates LPS-induced apoptosis via inhibiting NF-kB activity in chicken peripheral lymphocyte cultures

This study aims to investigate whether resveratrol (RES) could inhibit NF-κB activity and protect in vitro cultured chicken lymphocytes from apoptosis induced by continuous LPS stimulation. Blood lymphocytes of chickens were collected and cultured. LPS was added to the samples of treatment group, while the same volume of normal saline (NS) was supplemented to those of the control group. In the treatment groups, four different concentrations of RES (0, 20, 40, and 80 µg/ml) were admixed. Then, the following indicators were tested: lymphocyte apoptotic rate, lymphocyte viability, NF-κB activity, TNF-a level, reactive oxygen species (ROS), and expression of apoptosis-related proteins (Fas/FasL and Caspase-8). The results indicated that the application of different concentrations of RES could significantly increase the viability of lymphocytes and decrease the apoptotic rate (p<0.05) after continuous stimulations by LPS. The activity of NF-κB levels of TNF-a and ROS in the RES treatment subgroups was significantly decreased in comparison with that in the RES-blank subgroup (p<0.05). The cells in the treatment group that had been treated with 20, 40 and 80 μl/ml of RES exhibited a significantly lower Fas and Caspase-8 expression level than that in the RES-blank subgroup (p<0.05). These findings revealed that RES could substantially diminish the concentrations of ROS and TNF-a, down-regulate NF-κB activity, decrease the expression of Fas and Caspase-8, stimulate the activity of peripheral lymphocytes, and lower the rate of their apoptosis, induced by continuous LPS stimulation in chicken lymphocyte cultures.