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Front. Microbiol. | doi: 10.3389/fmicb.2019.00624

Impacts of duck-origin Parvovirus infection on Cherry Valley ducklings from the perspective of gut microbiota

 Qihui Luo1, 2*,  Jing Xu1, 2,  Chao Huang1, 2, Xinyu Lei1, 2, Dongjing Cheng1, Wengtao Liu1, 2,  Anchun Cheng1, Li Tang1, 2, Jing Fang1, Yangping Ou1,  Yi Geng1 and  Zhengli Chen1, 2
  • 1Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, China
  • 2Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, China

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.

Keywords: D-GPV, BADS, Gut microbiota dysbiosis, intestinal inflammation, SCFAs

Received: 07 Sep 2018; Accepted: 12 Mar 2019.

Edited by:

Souvik Ghosh, Ross University School of Veterinary Medicine, Saint Kitts and Nevis

Reviewed by:

Jakub Kreisinger, Charles University, Czechia
Felix N. Toka, Ross University School of Veterinary Medicine, Saint Kitts and Nevis  

Copyright: © 2019 Luo, Xu, Huang, Lei, Cheng, Liu, Cheng, Tang, Fang, Ou, Geng and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Qihui Luo, Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China, lqhbiology@163.com