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从肠道微生物群角度看鸭源细小病毒感染对樱桃谷鸭雏鸭的影响

Impacts of Duck-Origin Parvovirus Infection on Cherry Valley Ducklings From the Perspective of Gut Microbiota.

作者信息

Luo Qihui, Xu Jing, Huang Chao, Lei Xinyu, Cheng Dongjing, Liu Wentao, Cheng Anchun, Tang Li, Fang Jing, Ou Yangping, Geng Yi, Chen Zhengli

机构信息

Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

出版信息

Front Microbiol. 2019 Mar 28;10:624. doi: 10.3389/fmicb.2019.00624. eCollection 2019.

Abstract

Duck-origin goose parvovirus (D-GPV) is the causative agent of beak atrophy and dwarfism syndrome (BADS), characterized by growth retardation, skeletal dysplasia, and persistent diarrhea. However, the pathogenic mechanism of D-GPV remains undefined. Here, we first reported the gut microbiome diversity of D-GPV infected Cherry Valley ducks. In the investigation for the influence of D-GPV infection on gut microbiota through a period of infection, we found that D-GPV infection caused gut microbiota dysbiosis by reducing the prevalence of the dominant genera and decreasing microbial diversity. Furthermore, exfoliation of the intestinal epithelium, proliferation of lymphocytes, up-regulated mRNA expression of pro-inflammatory TNF-α, IL-1β, IL-6, IL-17A, and IL-22 and down-regulated mRNA expression of anti-inflammatory IL-10 and IL-4 occurred when D-GPV targeted in cecal epithelium. In addition, the content of short chain fatty acids (SCFAs) in cecal contents was significantly reduced after D-GPV infection. Importantly, the disorder of pro-inflammatory and anti-inflammatory cytokines was associated with the decrease of SCFAs-producing bacteria and the enrichment of opportunistic pathogens. Collectively, the decrease of SCFAs and the enrichment of pathogen-containing gut communities promoted intestinal inflammatory injury. These results may provide a new insight that target the gut microbiota to understand the progression of BADS disease and to research the pathogenic mechanism of D-GPV.

摘要

鸭源鹅细小病毒(D-GPV)是喙萎缩和侏儒症综合征(BADS)的病原体,其特征为生长迟缓、骨骼发育异常和持续性腹泻。然而,D-GPV的致病机制仍不明确。在此,我们首次报道了D-GPV感染的樱桃谷鸭的肠道微生物群多样性。在通过一段时间的感染来研究D-GPV感染对肠道微生物群的影响时,我们发现D-GPV感染通过降低优势菌属的流行率和减少微生物多样性导致肠道微生物群失调。此外,当D-GPV靶向盲肠上皮时,出现了肠上皮脱落、淋巴细胞增殖、促炎细胞因子TNF-α、IL-1β、IL-6、IL-17A和IL-22的mRNA表达上调以及抗炎细胞因子IL-10和IL-4的mRNA表达下调。另外,D-GPV感染后盲肠内容物中短链脂肪酸(SCFAs)的含量显著降低。重要的是,促炎和抗炎细胞因子的紊乱与产生SCFAs的细菌减少和机会性病原菌的富集有关。总的来说,SCFAs的减少和含病原体的肠道群落的富集促进了肠道炎症损伤。这些结果可能为针对肠道微生物群来理解BADS疾病的进展和研究D-GPV的致病机制提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef0a/6450226/7ce735d54d46/fmicb-10-00624-g001.jpg

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