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Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder

Diarrhea is considered to be associated with microbial dysbiosis caused by infection of pathogens but poorly understood. We herein characterized the colonic microbiota of diarrheal early-weaning piglets infected with porcine circovirus type 2 (PCV2) and Campylobacter. Campylobacter infection signifi...

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Autores principales: Yang, Gang, Yan, Yali, Zhang, Li, Ruan, Zheng, Hu, Xiaoqing, Zhang, Shuo, Li, Xiaozhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: KeAi Publishing 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503086/
https://www.ncbi.nlm.nih.gov/pubmed/33005770
http://dx.doi.org/10.1016/j.aninu.2020.05.003
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author Yang, Gang
Yan, Yali
Zhang, Li
Ruan, Zheng
Hu, Xiaoqing
Zhang, Shuo
Li, Xiaozhen
author_facet Yang, Gang
Yan, Yali
Zhang, Li
Ruan, Zheng
Hu, Xiaoqing
Zhang, Shuo
Li, Xiaozhen
author_sort Yang, Gang
collection PubMed
description Diarrhea is considered to be associated with microbial dysbiosis caused by infection of pathogens but poorly understood. We herein characterized the colonic microbiota of diarrheal early-weaning piglets infected with porcine circovirus type 2 (PCV2) and Campylobacter. Campylobacter infection significantly decreased species richness and Shannon diversity index of colonic microbiota together with a significant increase in the proportion of Campylobacter and Enterobacteriaceae, whereas no significant difference on the above indexes was observed in piglets infected with PCV2 compared with healthy piglets. PCV2 and Campylobacter infection could disturb the homeostasis of colonic microbiota through deterioration of ecological network within microbial community, and specially Campylobacter performed as a module hub in ecological networks. The microbial dysbiosis caused metabolic dysfunction and led to a remarkable reduction in production of short chain fatty acids, following by a higher pH level in colon cavity. Campylobacter infection disturbed the function of colonic tract barrier observed in terms of significant lower relative expression of claudin-1, occluding, and zonula occludens protein-1 genes, and PCV2 infection induced intestinal inflammation together with a higher permeability of colon. Generally, these results suggested that PCV2 and Campylobacter infection could induce microbial dysbiosis and metabolic dysfunction, and cause intestinal disorder, all of which finally were associated to contribute to the diarrhea of early-weaning piglets.
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spelling pubmed-75030862020-09-30 Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder Yang, Gang Yan, Yali Zhang, Li Ruan, Zheng Hu, Xiaoqing Zhang, Shuo Li, Xiaozhen Anim Nutr Original Research Article Diarrhea is considered to be associated with microbial dysbiosis caused by infection of pathogens but poorly understood. We herein characterized the colonic microbiota of diarrheal early-weaning piglets infected with porcine circovirus type 2 (PCV2) and Campylobacter. Campylobacter infection significantly decreased species richness and Shannon diversity index of colonic microbiota together with a significant increase in the proportion of Campylobacter and Enterobacteriaceae, whereas no significant difference on the above indexes was observed in piglets infected with PCV2 compared with healthy piglets. PCV2 and Campylobacter infection could disturb the homeostasis of colonic microbiota through deterioration of ecological network within microbial community, and specially Campylobacter performed as a module hub in ecological networks. The microbial dysbiosis caused metabolic dysfunction and led to a remarkable reduction in production of short chain fatty acids, following by a higher pH level in colon cavity. Campylobacter infection disturbed the function of colonic tract barrier observed in terms of significant lower relative expression of claudin-1, occluding, and zonula occludens protein-1 genes, and PCV2 infection induced intestinal inflammation together with a higher permeability of colon. Generally, these results suggested that PCV2 and Campylobacter infection could induce microbial dysbiosis and metabolic dysfunction, and cause intestinal disorder, all of which finally were associated to contribute to the diarrhea of early-weaning piglets. KeAi Publishing 2020-09 2020-07-18 /pmc/articles/PMC7503086/ /pubmed/33005770 http://dx.doi.org/10.1016/j.aninu.2020.05.003 Text en © 2020 Chinese Association of Animal Science and Veterinary Medicine. Production and hosting by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Research Article
Yang, Gang
Yan, Yali
Zhang, Li
Ruan, Zheng
Hu, Xiaoqing
Zhang, Shuo
Li, Xiaozhen
Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title_full Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title_fullStr Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title_full_unstemmed Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title_short Porcine circovirus type 2 (PCV2) and Campylobacter infection induce diarrhea in piglets: Microbial dysbiosis and intestinal disorder
title_sort porcine circovirus type 2 (pcv2) and campylobacter infection induce diarrhea in piglets: microbial dysbiosis and intestinal disorder
topic Original Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503086/
https://www.ncbi.nlm.nih.gov/pubmed/33005770
http://dx.doi.org/10.1016/j.aninu.2020.05.003
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