Li Zhifei, Yu Ermeng, Wang Guangjun, Yu Deguang, Zhang Kai, Gong Wangbao, Xie Jun
Key Laboratory of Tropical and Subtropical Fishery Resource Application and Cultivation, Pearl River Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, China.
Guangdong Ecological Remediation of Aquaculture Pollution Research Center, Guangzhou, China.
Front Microbiol. 2018 Aug 17;9:1913. doi: 10.3389/fmicb.2018.01913. eCollection 2018.
Constant consumption of broad bean ( L.) induces intestinal inflammation and reduces growth rate in grass carp ( C. et V). However, the mechanisms underlying these effects are unclear. In mammalian models of inflammatory bowel disease (IBD), endotoxin and flagellin cause intestinal inflammation through upregulation of tumor necrosis factor (TNF)-α expression. We therefore speculated that broad bean consumption alters intestinal microbiota composition, thereby increasing the relative abundance of endotoxin-producing Gram-negative and flagellated bacteria and resulting in upregulation of TNF-α and intestinal inflammation in grass carp. We tested this hypothesis by comparing intestinal microbiota compositions of grass carp fed broad bean (GCBB), hybrid giant napier ( Roxb, GCHG), or formula feed (GCFF) by 16S rRNA gene sequencing. We also performed a histological analysis of the intestinal inner wall by scanning electron microscopy and measured intestinal wall and serum concentrations of TNF-α. Our results revealed epithelial cell damage including microvillus effacement and synechia along with increased TNF-α levels in the intestinal wall in the GCBB group as compared to the GCHG and GCFF groups. The relative abundances of Gram-negative and flagellated bacteria were also higher in the GCBB group than in the GCHG and GCFF groups; this was accompanied by upregulation of genes expressing endotoxin and flagellin in intestinal microbiota. Thus, broad bean-induced intestinal inflammation in grass carp shares features with IBD. Our findings demonstrate that the microbiome in fish is directly influenced by diet and provide a reference for deconstructing host-intestinal microbiota interactions.
持续投喂蚕豆会诱发草鱼肠道炎症并降低其生长速度。然而，这些影响背后的机制尚不清楚。在炎症性肠病（IBD）的哺乳动物模型中，内毒素和鞭毛蛋白通过上调肿瘤坏死因子（TNF）-α的表达引发肠道炎症。因此，我们推测投喂蚕豆会改变草鱼肠道微生物群的组成，从而增加产生内毒素的革兰氏阴性菌和有鞭毛细菌的相对丰度，进而导致草鱼TNF-α上调和肠道炎症。我们通过16S rRNA基因测序比较了投喂蚕豆的草鱼（GCBB）、杂交狼尾草（Roxb，GCHG）或配合饲料（GCFF）的草鱼肠道微生物群组成，对这一假设进行了验证。我们还通过扫描电子显微镜对肠道内壁进行了组织学分析，并测量了肠壁和血清中TNF-α的浓度。我们的结果显示，与GCHG组和GCFF组相比，GCBB组的上皮细胞出现损伤，包括微绒毛消失和粘连，同时肠壁中TNF-α水平升高。GCBB组中革兰氏阴性菌和有鞭毛细菌的相对丰度也高于GCHG组和GCFF组；这伴随着肠道微生物群中表达内毒素和鞭毛蛋白的基因上调。因此，蚕豆诱导的草鱼肠道炎症与IBD有共同特征。我们的研究结果表明，鱼类的微生物群直接受饮食影响，并为解析宿主-肠道微生物群相互作用提供了参考。
