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一种由微生物群代谢产生的次级胆汁酸可减轻鸡亚临床坏死性肠炎中的回肠炎和胆汁酸减少。

A secondary bile acid from microbiota metabolism attenuates ileitis and bile acid reduction in subclinical necrotic enteritis in chickens.

作者信息

Bansal Mohit, Fu Ying, Alrubaye Bilal, Abraha Mussie, Almansour Ayidh, Gupta Anamika, Liyanage Rohana, Wang Hong, Hargis Billy, Sun Xiaolun

机构信息

1Center of Excellence for Poultry Science, University of Arkansas, 1260 W Maple St. O409, Fayetteville, AR 72701 USA.

2CEMB, University of Arkansas, Fayetteville, AR 72701 USA.

出版信息

J Anim Sci Biotechnol. 2020 Mar 13;11:37. doi: 10.1186/s40104-020-00441-6. eCollection 2020.

DOI:10.1186/s40104-020-00441-6
PMID:32190299
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7069026/
Abstract

BACKGROUND

-induced chicken necrotic enteritis (NE) is responsible for substantial economic losses worldwide annually. Recently, as a result of antibiotic growth promoter prohibition, the prevalence of NE in chickens has reemerged. This study was aimed to reduce NE through titrating dietary deoxycholic acid (DCA) as an effective antimicrobial alternative.

MATERIALS AND METHODS

Day-old broiler chicks were assigned to six groups and fed diets supplemented with 0 (basal diet), 0.8, 1.0 and 1.5 g/kg (on top of basal diet) DCA. The birds were challenged with (20,000 oocysts/bird) at d 18 and (10 CFU/bird per day) at d 23, 24, and 25 to induce NE. The birds were sacrificed at d 26 when ileal tissue and digesta were collected for analyzing histopathology, mRNA accumulation and colonization by real-time PCR, targeted metabolomics of bile acids, fluorescence hybridization (FISH), or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay.

RESULTS

At the cellular level, birds infected with and developed subclinical NE and showed shortening villi, crypt hyperplasia and immune cell infiltration in ileum. Dietary DCA alleviated the NE-induced ileal inflammation in a dose-dependent manner compared to NE control birds. Consistent with the increased histopathological scores, subclinical NE birds suffered body weight gain reduction compared to the uninfected birds, an effect attenuated with increased doses of dietary DCA. At the molecular level, the highest dose of DCA at 1.5 g/kg reduced luminal colonization compared to NE birds using PCR and FISH. Furthermore, the dietary DCA reduced subclinical NE-induced intestinal inflammatory gene expression and cell apoptosis using PCR and TUNEL assays. Upon further examining ileal bile acid pool through targeted metabolomics, subclinical NE reduced the total bile acid level in ileal digesta compared to uninfected birds. Notably, dietary DCA increased total bile acid and DCA levels in a dose-dependent manner compared to NE birds.

CONCLUSION

These results indicate that DCA attenuates NE-induced intestinal inflammation and bile acid reduction and could be an effective antimicrobial alternative against the intestinal disease.

摘要

背景

球虫诱导的鸡坏死性肠炎(NE)每年在全球造成巨大经济损失。近来,由于抗生素生长促进剂被禁用,鸡群中NE的发病率再次出现。本研究旨在通过滴定日粮脱氧胆酸(DCA)作为一种有效的抗菌替代品来降低NE的发病率。

材料与方法

将1日龄的肉鸡雏鸡分为6组,分别饲喂补充0(基础日粮)、0.8、1.0和1.5 g/kg(在基础日粮之上)DCA的日粮。在第18天用球虫(每只鸡20,000个卵囊)进行攻毒,并在第23、24和25天用产气荚膜梭菌(每只鸡每天10 CFU)进行攻毒以诱导NE。在第26天处死鸡,收集回肠组织和食糜,用于分析组织病理学、mRNA积累以及通过实时PCR、胆汁酸靶向代谢组学、荧光原位杂交(FISH)或末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)分析来检测产气荚膜梭菌的定植情况。

结果

在细胞水平上,感染球虫和产气荚膜梭菌的鸡出现亚临床NE,表现为回肠绒毛缩短、隐窝增生和免疫细胞浸润。与NE对照鸡相比,日粮DCA以剂量依赖的方式减轻了NE诱导的回肠炎症。与组织病理学评分增加一致,亚临床NE鸡与未感染鸡相比体重增加减少,日粮DCA剂量增加可减轻这种影响。在分子水平上,使用PCR和FISH检测,1.5 g/kg的最高剂量DCA与NE鸡相比减少了产气荚膜梭菌的肠腔定植。此外,日粮DCA使用PCR和TUNEL分析降低了亚临床NE诱导的肠道炎症基因表达和细胞凋亡。通过靶向代谢组学进一步检查回肠胆汁酸池时,与未感染鸡相比,亚临床NE降低了回肠食糜中的总胆汁酸水平。值得注意的是,与NE鸡相比,日粮DCA以剂量依赖的方式增加了总胆汁酸和DCA水平。

结论

这些结果表明,DCA减轻了NE诱导的肠道炎症和胆汁酸减少,可以作为预防肠道疾病的一种有效的抗菌替代品。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/57d8dcd10264/40104_2020_441_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/40828fdb6f0c/40104_2020_441_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/284a9a6771c0/40104_2020_441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/ae244e6b8610/40104_2020_441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/57d8dcd10264/40104_2020_441_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/40828fdb6f0c/40104_2020_441_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/4a291d4e6208/40104_2020_441_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/de8d210c2020/40104_2020_441_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/284a9a6771c0/40104_2020_441_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/ae244e6b8610/40104_2020_441_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6d7/7069026/57d8dcd10264/40104_2020_441_Fig6_HTML.jpg

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