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益生菌补充剂对实验性坏死性肠炎攻毒期间肉鸡生产性能和坏死性肠炎严重程度的影响。

Effect of synbiotic supplementation on production performance and severity of necrotic enteritis in broilers during an experimental necrotic enteritis challenge.

机构信息

Department of Poultry Science, University of Georgia, Athens, GA, USA.

Toxicology and Mycotoxin Research Unit, Agriculture Research Service, United States Department of Agriculture, Athens, GA, USA.

出版信息

Poult Sci. 2023 Oct;102(10):102959. doi: 10.1016/j.psj.2023.102959. Epub 2023 Jul 26.

DOI:10.1016/j.psj.2023.102959
PMID:37619505
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10470215/
Abstract

To evaluate the efficacy of synbiotic during a necrotic enteritis (NE) infection, a total of 360 day-old chicks were randomly assigned into 4 experimental groups in a 2 × 2 factorial setup: control, challenge, synbiotic (1 g/kg), and challenge + synbiotic, with 6 replicates. NE was induced by gavaging 1 × 10Eimeria maxima oocysts and 1 × 10 CFU/mL of Clostridium perfringens on d 14 (D14) and D19, 20, and 21, respectively. At D35, the NE challenge decreased the BW gain (P < 0.001) and increased feed conversion ratio (P = 0.03), whereas synbiotic supplementation decreased the feed intake (P = 0.04). At D21, NE challenge increased gut permeability (P < 0.001), decreased regulatory T cells (Tregs) in the cecal tonsil (CT) (P = 0.02), increased Tregs in the spleen (P = 0.02), decreased nitric oxide (NO) production in the spleen (P = 0.04) and decreased IL-10 expression in CT (P = 0.02), whereas synbiotic supplementation increased CD4+:CD8+ T cells in the spleen (P < 0.001) and decreased interferon (IFN)-γ expression in the jejunum (P = 0.07), however, synbiotic supplementation during NE challenge decreased mid-gut lesion score (P < 0.001), increased CD4+:CD8+ T cells in CT and decreased IgA production in bile (P < 0.001), compared to the control group. At D28, synbiotic supplementation decreased CD4+:CD8+ T cells in CT (P < 0.001), whereas synbiotic supplementation during NE challenge decreased Tregs in CT (P < 0.001) and increased NO production in the spleen (P = 0.04), compared to the control group. At D35, the NE challenge decreased CD4+:CD8+ T cells in the spleen (P = 0.03), decreased IgA production in bile (P = 0.02), decreased IL-10 expression in CT (P = 0.04), and decreased IL-10 (P = 0.009), IFN-γ (P = 0.03) and inducible nitric oxide synthase (P = 0.02) expression in the jejunum, whereas synbiotic supplementation increased Tregs in the spleen (P = 0.04), compared to control group. Synbiotic supplementation during the NE challenge decreased both IL-1β (P = 0.02) and IFN-γ (P = 0.001) expression in CT, compared to the control group. It can be concluded that synbiotic supplementation increases production performance by decreasing mid-gut lesions and enhancing protective immunity against NE, and efficiency of synbiotic could be improved by blending additional probiotics and prebiotics.

摘要

为了评估共生元在坏死性肠炎(NE)感染中的功效,将 360 只 1 日龄雏鸡随机分为 4 个实验组,采用 2×2 因子设计:对照组、攻毒组、共生元(1 g/kg)组和攻毒+共生元组,每组 6 个重复。在第 14 天(D14)和第 19 天,分别通过灌胃 1×10Eimeria maxima 卵囊和 1×10 CFU/mL 产气荚膜梭菌诱导 NE。在 D35,NE 攻毒降低了 BW 增益(P < 0.001)并增加了饲料转化率(P = 0.03),而共生元补充降低了采食量(P = 0.04)。在 D21,NE 攻毒增加了肠道通透性(P < 0.001),降低了盲肠扁桃体(CT)中的调节性 T 细胞(Tregs)(P = 0.02),增加了脾脏中的 Tregs(P = 0.02),降低了脾脏中的一氧化氮(NO)产生(P = 0.04)和 CT 中 IL-10 的表达(P = 0.02),而共生元补充增加了脾脏中的 CD4+:CD8+ T 细胞(P < 0.001)并降低了空肠中的干扰素(IFN)-γ表达(P = 0.07),然而,与对照组相比,在 NE 攻毒期间,共生元补充降低了中肠病变评分(P < 0.001),增加了 CT 中的 CD4+:CD8+ T 细胞,并降低了胆汁中的 IgA 产生(P < 0.001)。在 D28,共生元补充降低了 CT 中的 CD4+:CD8+ T 细胞(P < 0.001),而在 NE 攻毒期间,共生元补充降低了 CT 中的 Tregs(P < 0.001)并增加了脾脏中的 NO 产生(P = 0.04),与对照组相比。在 D35,NE 攻毒降低了脾脏中的 CD4+:CD8+ T 细胞(P = 0.03),降低了胆汁中的 IgA 产生(P = 0.02),降低了 CT 中的 IL-10 表达(P = 0.04)和 IL-10(P = 0.009)、IFN-γ(P = 0.03)和诱导型一氧化氮合酶(P = 0.02)在空肠中的表达,而与对照组相比,共生元补充增加了脾脏中的 Tregs(P = 0.04)。在 NE 攻毒期间,与对照组相比,共生元补充降低了 CT 中的 IL-1β(P = 0.02)和 IFN-γ(P = 0.001)的表达。可以得出结论,共生元补充通过降低中肠病变和增强对 NE 的保护性免疫来提高生产性能,并且通过混合额外的益生菌和益生元可以提高共生元的效率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/02506a128ef2/gr10.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/02506a128ef2/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/a73fde2c975f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/817ec1d427f0/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/e958511a4e01/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/c3df74971bda/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/44cfc6a2c3cb/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/4b55fda02bf0/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/0c84beb1d80f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/65b33ea6b543/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/444c023d9a45/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db90/10470215/02506a128ef2/gr10.jpg

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