Chicken amyloid arthropathy: serum amyloid A, interleukin-1beta, interleukin-6, tumour necrosis factor-alpha and nitric oxide profile in acute phase (12th hour).

Acute phase response (APR) is part of the early defense system, which is triggered by different stimuli including, infection, trauma, stres, inflammation and neoplasia. The APR complex is a reaction which induces homeostasis and recovery. In this research, serum amyloid A (SAA), interlaukin (IL)-1beta, IL-6, tumour necrosis factor alpha (TNF-alpha) and nitric oxide (NO) levels were measured 12 hours following injection. For this purpose, Thirty-two 5 weeks old laying chicken were allocated into four groups and intra-articular injections of Freund's adjuvant were used to induce amylod arthropathy in Groups II, III and IV. Vitamin A in group II, and methylprednisolone in group IV were added to enhance and to reduce the severity of amyloidosis, respectively. At the end of the research, it was observed that TNF-alpha and NO increased significantly (P < 0.05) in vitamin A and methylprednisolone groups whereas SAA decreased significantly (P < 0.05) in all groups. It was also observed that IL-6 increased (P < 0.05) in vitamin A group and decreased in all other gorups however, IL-1beta decreased in vitamin A and methylprednisolone groups, while it was increased in the control group. The results of this study suggest that there is a positive correlation between serum TNF-alpha levels in acute and chronic phase in chickens with amyloid arthropathy.

Matrix metalloproteinase, vitamin A and methylprednisolone effects on experimentally induced amyloid arthropathy.

We evaluated the role of some matrix metalloproteinases (MMPs) in enhancing the effect of vitamin A and the inhibiting effect of methylprednisolone on amyloid arthropathy in brown layer chicks. We used 100 one-day-old Isa brown layer chicks. The chicks were allocated to one of four groups as follows: negative control group (I), vitamin A group (II), positive control group (III) and methylprednisolone group (IV). Amyloid arthropathy was induced by injections of complete Freund's adjuvant into the left intertarsal joints of the chicks. Serum vitamin A and tissue MMP (MMP-1, MMP-2, MMP-9) levels were measured and differences among the groups were investigated. Serum vitamin A rates (µg/dl) were: 63.57 ± 4.10, 47.13 ± 10.62, 53.26 ± 10.79, 98.48 ± 8.20 in groups I, II, III and IV, respectively (p < 0.001). MMP-1, MMP-2 and MMP-9 levels were evaluated in tissues from the chickens with amyloid arthropathy. Methylprednisolone significantly suppressed the release of MMP-1 and MMP-2, and increased the release of MMP-9 in birds with amyloid arthropathy. In addition, vitamin A significantly increased the release of MMP-1, MMP-2 and MMP-9.

The effect of dietary supplementation of nitric oxide donor and inhibitor on nNOS expression in and motility of the small intestine of broilers.

We investigated the effect of dietary supplementation of sodium nitroprusside (SNP), a nitric oxide (NO) donor, and N-nitro-L-arginine methyl ester (L-NAME), a NO inhibitor, on neuronal nitric oxide synthase (nNOS) expression in and motility of small intestinum in broilers. A total of 560, one-day-old Ross 308 hybrid mixed sex broiler chicks were divided randomly into one control and seven treatment groups for a 42 day feeding trial including starter phase (0-21 days) and grower phase (22-42 days). The control group was fed a basal diet and the experimental groups were the fed basal diet supplemented with 25, 50, 100 and 200 mg/kg SNP and 25, 50 or 100 mg/kg L-NAME. Ten chickens from each group were sacrificed to collect samples on days 21 and 42. The expression patterns of nNOS immunoreactivity in nerve fibers were determined by immunohistochemistry. In the contractility studies, longitudinal isolated strips of duodenum, jejunum and ileum were treated with 10(-5) M L-arginine and 10(-4) M SNP. Immunohistochemistry revealed that nNOS expression was not detectable in the duodenum or ileum of either the control or experimental groups. On the other hand, nNOS immunoreactivity in the jejunum control group showed a strong reaction on day 21, but the reaction was weak on day 42. nNOS expression clearly was suppressed on day 21 by the diet supplemented with L-NAME, while the diet supplemented with SNP stimulated nNOS expression on day 21. Contractility experiments revealed that spontaneous contractility of isolated strips of duodenum, jejunum and ileum showed no significant difference among groups. Spontaneous contractions of all strips were inhibited by L-arginine and SNP in all groups. The percentage inhibition rate of spontaneous contractions of jejunum application on days 21 and 42 after L-arginine decreased in the group supplemented with 100 mg/kg L-NAME. The percentage inhibition rate on day 21 after SNP application decreased in both groups that received 50 and 100 mg/kg L-NAME. We demonstrated the expression pattern of nNOS in nerve fibers in jejunum of broiler chickens. Contractility studies revealed that the NOS-NO pathway may play a role in smooth muscle contraction of small intestine of chickens. Feeding strategies that supplement NO donor and NO inhibitor can be of physiological importance to small intestine motility owing to alteration of nNOS expression in the jejunum.