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.
Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
Poult Sci. 2021 Apr;100(4):101021. doi: 10.1016/j.psj.2021.101021. Epub 2021 Jan 28.
Duck-origin parvovirus disease is an epidemic disease mainly caused by duck-origin goose parvovirus (D-GPV), which is characterized by beak atrophy and dwarfism syndrome. Its main symptoms are persistent diarrhea, skeletal dysplasia, and growth retardation. However, the pathogenesis of Cherry Valley ducks infected by D-GPV has not been studied thoroughly. To perceive the distribution of D-GPV in the intestinal tract, intestinal morphological development, intestinal permeability, inflammatory cytokines in Cherry Valley ducks, and expression of tight junction protein, the D-GPV infection was given intramuscularly. Illumina MiSeq sequencing technology was used to analyze the diversity and structure of ileum flora and content of short-chain fatty acids of its metabolites. To investigate the relationship between intestinal flora changes and intestinal barrier function after D-GPV infection on Cherry Valley ducks is of great theoretical and practical significance for further understanding the pathogenesis of D-GPV and the structure of intestinal flora in ducks. The results showed that D-GPV infection was accompanied by intestinal inflammation and barrier dysfunction. At this time, the decrease of a large number of beneficial bacteria and the content of short-chain fatty acids in intestinal flora led to the weakening of colonization resistance of the intestinal flora and the accumulation of potentially pathogenic bacteria, which would aggravate the negative effect of D-GPV damage to the intestinal tract. Furthermore, a significant increase in Unclassified_S24-7 and decrease in Streptococcus was observed in D-GPV persistent, indicating the disruption in the structure of gut microbiota. Notably, the shift of microbiota was associated with the transcription of tight-junction protein and immune-associated cytokines. These results indicate that altered ileum microbiota, intestinal barrier, and immune dysfunction are associated with D-GPV infection. Therefore, there is a relationship between the intestinal barrier dysfunction and dysbiosis caused by D-GPV, but the specific mechanism needs to be further explored.
鸭源细小病毒病是一种主要由鸭源鹅细小病毒（D-GPV）引起的传染病，其特征为喙萎缩和侏儒综合征。主要症状为持续性腹泻、骨骼发育不良和生长迟缓。然而，感染 D-GPV 的樱桃谷鸭的发病机制尚未得到深入研究。为了感知 D-GPV 在樱桃谷鸭肠道中的分布、肠道形态发育、肠道通透性、炎症细胞因子和紧密连接蛋白的表达，采用肌肉注射的方式感染 D-GPV。利用 Illumina MiSeq 测序技术分析其回肠菌群的多样性和结构以及短链脂肪酸代谢物的含量。研究 D-GPV 感染樱桃谷鸭后肠道菌群变化与肠道屏障功能的关系，对于进一步了解 D-GPV 的发病机制和鸭肠道菌群结构具有重要的理论和实践意义。结果表明，D-GPV 感染伴随着肠道炎症和屏障功能障碍。此时，大量有益菌和肠道菌群中短链脂肪酸含量的减少导致了菌群定植抵抗力的减弱和潜在致病菌的积累，从而加剧了 D-GPV 对肠道的损伤的负面影响。此外，在 D-GPV 持续感染时，观察到未分类_S24-7 的显著增加和链球菌的减少，表明肠道微生物群结构的破坏。值得注意的是，微生物群的移位与紧密连接蛋白和免疫相关细胞因子的转录有关。这些结果表明，改变的回肠微生物群、肠道屏障和免疫功能障碍与 D-GPV 感染有关。因此，D-GPV 引起的肠道屏障功能障碍和菌群失调之间存在关联，但具体机制仍需进一步探讨。
