猕猴慢性腹泻中的菌群-宿主互作机制
创作:大力 审核:mildbreeze 2019年03月31日
  • 宏转录组学分析表明,特发性慢性腹泻(ICD)猕猴中,宿主炎症相关基因表达增加,肠道菌群多样性降低,普氏菌以及弯曲杆菌、螺杆菌、毛滴虫等病原体的转录产物增多;
  • ICD菌群中降解黏蛋白的菌和酶的基因表达增加,提示ICD菌群能降解粘液屏障;
  • ICD宿主肠细胞合成的岩藻糖化粘蛋白增多,伴随菌群对岩藻糖的利用发生变化,促进致病菌生存:拟杆菌可通过裂解将岩藻糖提供给普氏菌和嗜血杆菌作为碳源,而弯曲杆菌可将岩藻糖作为黏附位点。
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mildbreeze
《Microbiome》近期发表的一项研究,通过粪便宏转录组学方法,分析了恒河猴特发性慢性腹泻(ICD)中的宿主和肠道菌群的基因表达变化,表明ICD肠道菌群中,致病菌基因表达增加、黏蛋白降解作用增强、对岩藻糖的利用发生改变,而宿主生成的岩藻糖基化黏蛋白,可被菌群中的潜在致病菌作为碳源或黏附位点所利用,从而促进疾病。这些发现对于研究肠道疾病中的菌群-宿主互作机制,有参考意义。
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Microbiome [IF:14.65]

Fecal metatranscriptomics of macaques with idiopathic chronic diarrhea reveals altered mucin degradation and fucose utilization

特发性慢性腹泻猕猴的粪便宏转录组学揭示粘蛋白降解和岩藻糖利用发生变化

10.1186/s40168-019-0664-z

2019-03-18, Article

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BACKGROUND: Idiopathic chronic diarrhea (ICD) is a common cause of morbidity and mortality among juvenile rhesus macaques. Characterized by chronic inflammation of the colon and repeated bouts of diarrhea, ICD is largely unresponsive to medical interventions, including corticosteroid, antiparasitic, and antibiotic treatments. Although ICD is accompanied by large disruptions in the composition of the commensal gut microbiome, no single pathogen has been concretely identified as responsible for the onset and continuation of the disease.
RESULTS: Fecal samples were collected from 12 ICD-diagnosed macaques and 12 age- and sex-matched controls. RNA was extracted for metatranscriptomic analysis of organisms and functional annotations associated with the gut microbiome. Bacterial, fungal, archaeal, protozoan, and macaque (host) transcripts were simultaneously assessed. ICD-afflicted animals were characterized by increased expression of host-derived genes involved in inflammation and increased transcripts from bacterial pathogens such as Campylobacter and Helicobacter and the protozoan Trichomonas. Transcripts associated with known mucin-degrading organisms and mucin-degrading enzymes were elevated in the fecal microbiomes of ICD-afflicted animals. Assessment of colon sections using immunohistochemistry and of the host transcriptome suggests differential fucosylation of mucins between control and ICD-afflicted animals. Interrogation of the metatranscriptome for fucose utilization genes reveals possible mechanisms by which opportunists persist in ICD. Bacteroides sp. potentially cross-fed fucose to Haemophilus whereas Campylobacter expressed a mucosa-associated transcriptome with increased expression of adherence genes.
CONCLUSIONS: The simultaneous profiling of bacterial, fungal, archaeal, protozoan, and macaque transcripts from stool samples reveals that ICD of rhesus macaques is associated with increased gene expression by pathogens, increased mucin degradation, and altered fucose utilization. The data suggest that the ICD-afflicted host produces fucosylated mucins that are leveraged by potentially pathogenic microbes as a carbon source or as adhesion sites.

First Authors:
Samuel T Westreich

Correspondence Authors:
Danielle G Lemay

All Authors:
Samuel T Westreich,Amir Ardeshir,Zeynep Alkan,Mary E Kable,Ian Korf,Danielle G Lemay

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