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日粮有机酸通过恢复肉鸡肠道微生物群来减轻高饲养密度应激诱导的肠道炎症。

Dietary organic acids ameliorate high stocking density stress-induced intestinal inflammation through the restoration of intestinal microbiota in broilers.

作者信息

Dai Dong, Qi Guanghai, Wang Jing, Zhang Haijun, Qiu Kai, Han Yanming, Wu Yuanyuan, Wu Shugeng

机构信息

Laboratory of Quality and Safety Risk Assessment for Animal Products on Feed Hazards (Beijing) of the Ministry of Agriculture and Rural Affairs, Institute of Feed Research, Chinese Academy of Agricultural Sciences, No. 12 Zhongguancun South St., Haidian district, Beijing, China.

Trouw Nutrition Research & Development Centers, Amersfoort, Netherlands.

出版信息

J Anim Sci Biotechnol. 2022 Nov 14;13(1):124. doi: 10.1186/s40104-022-00776-2.

DOI:10.1186/s40104-022-00776-2
PMID:36372893
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9661804/
Abstract

BACKGROUND

High stocking density (HSD) stress has detrimental effects on growth performance, intestinal barrier function, and intestinal microbiota in intensive animal production. Organic acids (OA) are widely used as feed additives for their ability to improve growth performance and intestinal health in poultry. However, whether dietary OA can ameliorate HSD stress-induced impaired intestinal barrier in broilers remains elusive. In this study, a total of 528 one-day-old male Arbor Acres broilers were randomly allocated into 3 treatments with 12 replicates per treatment including 10 birds for normal stocking density and 17 birds for HSD. The dietary treatments were as follows: 1) Normal stocking density + basal diet; 2) HSD + basal diets; 3) HSD + OA.

RESULTS

HSD stress can induce increased levels of serum corticosterone, lipopolysaccharides, interleukin-1β, tumor necrosis factor-α, and down-regulated mRNA expression of ZO-1, resulting in compromised growth performance of broilers (P < 0.05). Dietary OA could significantly reduce levels of serum corticosterone, lipopolysaccharides, interleukin-1β, and tumor necrosis factor-α, which were accompanied by up-regulated interleukin-10, mRNA expression of ZO-1, and growth performance (P < 0.05). Moreover, OA could down-regulate the mRNA expression of TLR4 and MyD88 to inhibit the NF-κB signaling pathway (P < 0.05). Additionally, HSD stress significantly decreased the abundance of Bacteroidetes and disturbed the balance of microbial ecosystems, whereas OA significantly increased the abundance of Bacteroidetes and restored the disordered gut microbiota by reducing competitive and exploitative interactions in microbial communities (P < 0.05). Meanwhile, OA significantly increased the content of acetic and butyric acids, which showed significant correlations with intestinal inflammation indicators (P < 0.05).

CONCLUSIONS

Dietary OA ameliorated intestinal inflammation and growth performance of broilers through restoring the disordered gut microbial compositions and interactions induced by HSD and elevating short-chain fatty acid production to inhibit the TLR4/NF-κB signaling pathway. These findings demonstrated the critical role of intestinal microbiota in mediating the HSD-induced inflammatory responses, contributing to exploring nutritional strategies to alleviate HSD-induced stress in animals.

摘要

背景

在集约化动物生产中,高饲养密度(HSD)应激对生长性能、肠道屏障功能和肠道微生物群具有不利影响。有机酸(OA)因其能够改善家禽生长性能和肠道健康而被广泛用作饲料添加剂。然而,日粮中的OA是否能改善HSD应激诱导的肉鸡肠道屏障受损仍不清楚。在本研究中,总共528只1日龄雄性艾维茵肉鸡被随机分为3组处理,每组处理12个重复,其中正常饲养密度组每组10只鸡,HSD组每组17只鸡。日粮处理如下:1)正常饲养密度+基础日粮;2)HSD+基础日粮;3)HSD+OA。

结果

HSD应激可导致血清皮质酮、脂多糖、白细胞介素-1β、肿瘤坏死因子-α水平升高,紧密连接蛋白1(ZO-1)的mRNA表达下调,导致肉鸡生长性能受损(P<0.05)。日粮OA可显著降低血清皮质酮、脂多糖、白细胞介素-1β和肿瘤坏死因子-α水平,同时伴随着白细胞介素-10、ZO-1的mRNA表达上调以及生长性能的改善(P<0.05)。此外,OA可下调Toll样受体4(TLR4)和髓样分化因子88(MyD88)的mRNA表达,从而抑制核因子κB(NF-κB)信号通路(P<0.05)。另外,HSD应激显著降低拟杆菌门的丰度并扰乱微生物生态系统的平衡,而OA显著增加拟杆菌门的丰度,并通过减少微生物群落中的竞争和剥削性相互作用来恢复紊乱的肠道微生物群(P<0.05)。同时,OA显著增加乙酸和丁酸的含量,其与肠道炎症指标呈显著相关性(P<0.05)。

结论

日粮OA通过恢复HSD诱导的紊乱肠道微生物组成和相互作用以及提高短链脂肪酸产量以抑制TLR4/NF-κB信号通路,从而改善肉鸡肠道炎症和生长性能。这些发现证明了肠道微生物群在介导HSD诱导的炎症反应中的关键作用,有助于探索缓解动物HSD诱导应激的营养策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/ba74d861ff32/40104_2022_776_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/ba74d861ff32/40104_2022_776_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/b34ef3726f67/40104_2022_776_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/6098a27e6bcf/40104_2022_776_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/74b41bff18cb/40104_2022_776_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/0cc99650d634/40104_2022_776_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b38/9661804/ba74d861ff32/40104_2022_776_Fig6_HTML.jpg

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