Avian Influenza Virus Subtype H9N2 Affects Intestinal Microbiota, Barrier Structure Injury, and Inflammatory Intestinal Disease in the Chicken Ileum
文献类型: 外文期刊
作者: Li, Hongxin 1 ; Liu, Xiaolin 1 ; Chen, Feiyang 1 ; Zuo, Kejing 5 ; Wu, Che 1 ; Yan, Yiming 1 ; Chen, Weiguo 1 ; Lin, Wenc 1 ;
作者机构: 1.South China Agr Univ, Coll Anim Sci, Guangzhou 510642, Guangdong, Peoples R China
2.Minist Agr, Key Lab Chicken Genet Breeding & Reprod, Guangzhou 510642, Guangdong, Peoples R China
3.Key Lab Anim Hlth Aquaculture & Environm Control, Guangzhou 510642, Guangdong, Peoples R China
4.Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Guangzhou 510642, Guangdong, Peoples R China
5.Guangzhou Zoo, Vet Lab, Guangzhou 510642, Guangdong, Peoples R China
6.South China Collaborat Innovat Ctr Poultry Dis Co, Guangzhou 510642, Guangdong, Peoples R China
关键词: H9N2 AIV; intestinal microbiota; barrier injury; inflammatory intestinal disease; E. coli
期刊名称:VIRUSES-BASEL ( 影响因子:5.048; 五年影响因子:5.127 )
ISSN: 1999-4915
年卷期: 2018 年 10 卷 5 期
页码:
收录情况: SCI
摘要: Avian influenza virus subtype H9N2 (H9N2 AIV) has caused significant losses to the poultry industry due to the high mortality associated with secondary infections attributable to E. coli. This study tries to address the underlying secondary mechanisms after H9N2 AIV infection. Initially, nine day-old specific pathogen-free chickens were assigned to control (uninfected) and H9N2-infected groups, respectively. Using Illumina sequencing, histological examination, and quantitative real-time PCR, it was found that H9N2 AIV caused intestinal microbiota disorder, injury, and inflammatory damage to the intestinal mucosa. Notably, the genera Escherichia, especially E. coli, significantly increased (p < 0.01) at five days post-infection (dpi), while Lactobacillus, Enterococcus, and other probiotic organisms were significantly reduced (p < 0.01). Simultaneously, the mRNA expression of tight junction proteins (ZO-1, claudin 3, and occludin), TFF2, and Muc2 were significantly reduced (p < 0.01), indicating the destruction of the intestinal epithelial cell tight junctions and the damage of mucin layer construction. Moreover, the mRNA expression of proinflammatory cytokines IFN-, IL-22, IFN-, and IL-17A in intestinal epithelial cells were significantly upregulated, resulting in the inflammatory response and intestinal injury. Our findings may provide a theoretical basis for observed gastroenteritis-like symptoms such as diarrhea and secondary E. coli infection following H9N2 AIV infection.
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