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Host responses to Clostridium perfringens challenge in a chicken model of chronic stress.
Gut Pathogens ( IF 4.2 ) Pub Date : 2020-05-06 , DOI: 10.1186/s13099-020-00362-9
Sarah J M Zaytsoff 1, 2 , Sarah M Lyons 3 , Alexander M Garner 4 , Richard R E Uwiera 2 , Wesley F Zandberg 3, 5 , D Wade Abbott 1 , G Douglas Inglis 1
Affiliation  

Background This study utilized a chicken model of chronic physiological stress mediated by corticosterone (CORT) administration to ascertain how various host metrics are altered upon challenge with Clostridium perfringens. Necrotic enteritis (NE) is a disease of the small intestine of chickens incited by C. perfringens, which can result in elevated morbidity and mortality. The objective of the current study was to investigate how physiological stress alters host responses and predisposes birds to subclinical NE. Results Birds administered CORT exhibited higher densities of C. perfringens in their intestine, and this corresponded to altered production of intestinal mucus. Characterization of mucus showed that C. perfringens treatment altered the relative abundance of five glycans. Birds inoculated with C. perfringens did not exhibit evidence of acute morbidity. However, histopathologic changes were observed in the small intestine of infected birds. Birds administered CORT showed altered gene expression of tight junction proteins (i.e. CLDN3 and CLDN5) and toll-like receptors (i.e. TLR2 and TLR15) in the small intestine. Moreover, birds administered CORT exhibited increased expression of IL2 and G-CSF in the spleen, and IL1β, IL2, IL18, IFNγ, and IL6 in the thymus. Body weight gain was impaired only in birds that were administered CORT and challenged with C. perfringens. Conclusion CORT administration modulated a number of host functions, which corresponded to increased densities of C. perfringens in the small intestine and weight gain impairment in chickens. Importantly, results implicate physiological stress as an important predisposing factor to NE, which emphasizes the importance of managing stress to optimize chicken health.

中文翻译:

慢性应激鸡模型中宿主对产气荚膜梭菌挑战的反应。

背景 本研究利用由皮质酮 (CORT) 给药介导的慢性生理应激的鸡模型来确定各种宿主指标在受到产气荚膜梭菌攻击时如何改变。坏死性肠炎 (NE) 是一种由产气荚膜梭菌引起的鸡小肠疾病,可导致发病率和死亡率升高。本研究的目的是调查生理压力如何改变宿主反应并使鸟类易患亚临床 NE。结果 施用 CORT 的鸟类在其肠道中表现出更高的产气荚膜梭菌密度,这与肠道粘液的产生变化相对应。粘液的表征表明产气荚膜梭菌处理改变了五种聚糖的相对丰度。接种 C. perfringens 没有表现出急性发病率的证据。然而,在受感染禽类的小肠中观察到组织病理学变化。施用 CORT 的鸡只显示小肠中紧密连接蛋白(即 CLDN3 和 CLDN5)和 toll 样受体(即 TLR2 和 TLR15)的基因表达发生了改变。此外,施用 CORT 的鸡只表现出脾脏中 IL2 和 G-CSF 以及胸腺中 IL1β、IL2、IL18、IFNγ 和 IL6 的表达增加。仅在使用 CORT 并用产气荚膜梭菌攻击的鸡只中体重增加受损。结论 CORT 给药调节了许多宿主功能,这对应于小肠中产气荚膜梭菌密度的增加和鸡的体重增加障碍。重要的,
更新日期:2020-05-06
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