Dysbiosis of Gut Microbiota and Intestinal Barrier Dysfunction in Pigs with Pulmonary Inflammation Induced by Mycoplasma hyorhinis Infection
文献类型: 外文期刊
作者: Zhang, Yingying 1 ; Gan, Yuan 2 ; Wang, Jia 2 ; Feng, Zhixin 2 ; Zhong, Zhaoxin 3 ; Bao, Hongduo 1 ; Xiong, Qiyan 2 ; Wang, Ran 1 ;
作者机构: 1.Jiangsu Acad Agr Sci, Inst Food Safety & Nutr, Key Lab Food Qual & Safety Jiangsu Prov, State Key Lab Breeding Base, Nanjing, Peoples R China
2.Jiangsu Acad Agr Sci, Inst Vet Med, Key Lab Vet Bioprod Engn, Minist Agr & Rural Affairs, Nanjing, Peoples R China
3.Jiangsu Coastal Area Inst Agr Sci, Yancheng, Peoples R China
关键词: Mycoplasma hyorhinis; gut microbiota; proteomics; barrier function; gut-lung axis
期刊名称:MSYSTEMS ( 影响因子:7.324; 五年影响因子:9.039 )
ISSN: 2379-5077
年卷期:
页码:
收录情况: SCI
摘要: Lung inflammation induced by Mycoplasma hyorhinis infection accounts for significant economic losses in the swine industry. Increasing evidence suggests that there is cross talk between the lungs and the gut, but little is known about the effect of the lung inflammation caused by M. hyorhinis infection on gut microbiota and intestinal barrier function. Here, we investigated changes in the fecal microbiotas of pigs with M. hyorhinis infection and the microbial regulatory role of such infection in intestinal barrier function. We infected pigs with M. hyorhinis and performed 16S rRNA gene sequencing analyses of fecal samples, data-independent acquisition (DIA) quantitative proteomic analyses of intestinal mucosa, and analyses of barrier dysfunction indicators in serum. We found that pigs with M. hyorhinis infection exhibit lung and systemic inflammation, as reflected by the histopathological changes and activation of the TLR4/MyD88/NF-kappa B p65 signaling pathway in lung tissue, as well as the increased concentrations of serum inflammatory cytokines. Gut microbiotas tended to become disturbed, as evidenced by the enrichment of opportunistic pathogens. The increased diamine oxidase activities and D-lactate concentrations in serum and the decreased relative mRNA expression of Occludin, ZO-1, and Mucin2 indicated the impairment of intestinal barrier function. Quantitative proteomic analyses showed a variety of altered proteins involved in immunomodulatory and inflammatory functions. There was a positive correlation between the abundance of opportunistic pathogens and inflammatory-cytokine concentrations, as well as intestinal immunomodulatory proteins. Our results suggest that lung inflammation induced by M. hyorhinis infection can contribute to the dysbiosis of gut microbiota and intestinal barrier dysfunction, and dysbiosis of gut microbiota was associated with systemic inflammation and intestinal immune status. IMPORTANCE Cumulative evidence suggests that bacterial pneumonia may contribute to the dysbiosis of the gut microbiota and other gastrointestinal symptoms. Our experiment has demonstrated that lung inflammation induced by M. hyorhinis infection was associated with gut microbiota dysbiosis and intestinal barrier dysfunction, which may provide a theoretical basis for exploring the gut-lung axis based on M. hyorhinis infection.
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