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首页> 外文期刊>Journal of Animal Science >Acute heat stress impairs performance parameters and induces mild intestinal enteritis in broiler chickens: Role of acute hypothalamic-pituitary-adrenal axis activation
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Acute heat stress impairs performance parameters and induces mild intestinal enteritis in broiler chickens: Role of acute hypothalamic-pituitary-adrenal axis activation

机译:急性热应激会损害肉鸡的性能参数并诱发轻度肠道肠炎:急性下丘脑-垂体-肾上腺轴激活的作用

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摘要

Studies on the environmental consequences of stress are relevant for economic and animal welfare reasons. We recently reported that long-term heat stressors (31 +/- 1 degrees C and 36 +/- 1 degrees C for 10 h/d) applied to broiler chickens (Gallus gallus domesticus) from d 35 to 42 of life increased serum corticosterone concentrations, decreased performance variables and the macrophage oxidative burst, and produced mild, multifocal acute enteritis. Being cognizant of the relevance of acute heat stress on tropical and subtropical poultry production, we designed the current experiment to analyze, from a neuroimmune perspective, the effects of an acute heat stress (31 +/- 1 degrees C for 10 h on d 35 of life) on serum corticosterone, performance variables, intestinal histology, and peritoneal macrophage activity in chickens. We demonstrated that the acute heat stress increased serum corticosterone concentrations and mortality and decreased food intake, BW gain, and feed conversion (P < 0.05). We did not find changes in the relative weights of the spleen, thymus, and bursa of Fabricius (P > 0.05). Increases in the basal and the Staphylococcus aureus-induced macrophage oxidative bursts and a decrease in the percentage of macrophages performing phagocytosis were also observed. Finally, mild, multifocal acute enteritis, characterized by the increased presence of lymphocytes and plasmocytes within the lamina propria of the jejunum, was also observed. We found that the stress-induced hypothalamic-pituitary-adrenal axis activation was responsible for the negative effects observed on chicken performance and immune function as well as for the changes in the intestinal mucosa. The data presented here corroborate with those presented in other studies in the field of neuroimmunomodulation and open new avenues for the improvement of broiler chicken welfare and production performance.
机译:出于经济和动物福利原因,对压力对环境造成的影响的研究是相关的。我们最近报告说,从生命的第35天到第42天,长期热应激(31 +/- 1摄氏度和36 +/- 1摄氏度,持续10 h / d)施加于肉鸡(Gallus gallus domesticus),会使血清皮质酮增加浓度降低,性能变量降低和巨噬细胞氧化爆发,并产生轻度,多灶性急性肠炎。考虑到急性热应激与热带和亚热带家禽生产的相关性,我们设计了当前实验,从神经免疫角度分析了急性热应激(31 +/- 1摄氏度,持续10 h对d 35的影响)寿命)对鸡血清皮质酮,性能变量,肠道组织学和腹膜巨噬细胞活性的影响。我们证明了急性热应激会增加血清皮质酮的浓度和死亡率,并减少食物摄入,体重增加和饲料转化率(P <0.05)。我们没有发现Fabricius的脾脏,胸腺和法氏囊的相对重量发生变化(P> 0.05)。还观察到基底和金黄色葡萄球菌诱导的巨噬细胞氧化爆发增加,并且巨噬细胞进行吞噬作用的百分比降低。最后,还观察到轻度,多灶性急性肠炎,其特征在于空肠固有层内淋巴细胞和浆细胞的存在增加。我们发现,应激诱导的下丘脑-垂体-肾上腺轴活化是造成鸡性能和免疫功能下降以及肠道粘膜变化的原因。本文提供的数据与神经免疫调节领域其他研究中提供的数据相符,并为改善肉鸡的福利和生产性能开辟了新途径。

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