Wang Rundong, Deng Yijia, Deng Qi, Sun Dongfang, Fang Zhijia, Sun Lijun, Wang Yaling, Gooneratne Ravi
College of Food Science and Technology, Guangdong Ocean University, Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Key Laboratory of Advanced Processing of Aquatic Products of Guangdong Higher Education Institution, Zhanjiang, China.
School of Chemistry and Chemical Engineering, Key Laboratory of Clean Energy Materials Chemistry of Guangdong Higher Education Institutes, Lingnan Normal University, Zhanjiang, China.
Front Microbiol. 2020 Jan 30;11:73. doi: 10.3389/fmicb.2020.00073. eCollection 2020.
(Vp), a major food-borne pathogen, is responsible for severe infections such as gastroenteritis and septicemia, which may be accompanied by life-threatening complications. While studies have evaluated factors that affect the virulence of the pathogen, none have investigated the interaction of Vp with gut microbiota. To address this knowledge gap, we compared the effect of Vp on gut bacterial community structure, immunity, liver and kidney function, in pseudo germ-free (PGF) mice and normal (control) mice. Significant damage to the ileum was observed in normal mice compared with the PGF mice. The inflammatory factors IL-1β, IL-6, and TNF-α in normal mice were ∼2.5-fold higher than in the PGF mice, and liver (ALT, AST, ALP) and kidney (BUN) function indices were ∼1.6-fold higher. The Vp infection substantially reduced species composition and richness of the gut microbial communities. In particular, there was a shift in keystone taxa, from protective species of genera , , , and in the gut of control mice to opportunistic pathogens , , , and in Vp-infected mice, thus affecting microbiota-related biological functions in the mice. Specifically, pathways involved in infectious diseases and ion channels were significantly augmented in infected mice, while the pathways involved in metabolism, digestion and cell growth declined. We propose that the normal mice are more prone to Vp infection because of the alteration in gut-microbe-mediated functions. All these effects reduce intestinal resistance, with marked damage to the gut lining and pathogen leakage into the blood culminating in liver and kidney damage. These findings greatly advance our understanding of the mechanisms underlying interactions between Vp, the gut microbiota and the infected host.
副溶血性弧菌（Vp）是一种主要的食源性病原体，可导致严重感染，如肠胃炎和败血症，可能伴有危及生命的并发症。虽然已有研究评估了影响该病原体毒力的因素，但尚无研究调查Vp与肠道微生物群的相互作用。为填补这一知识空白，我们比较了Vp对无菌小鼠（PGF）和正常（对照）小鼠肠道细菌群落结构、免疫力、肝脏和肾脏功能的影响。与PGF小鼠相比，正常小鼠的回肠出现了明显损伤。正常小鼠体内的炎症因子白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）比PGF小鼠高约2.5倍，肝脏（谷丙转氨酶、谷草转氨酶、碱性磷酸酶）和肾脏（尿素氮）功能指标高约1.6倍。Vp感染显著降低了肠道微生物群落的物种组成和丰富度。特别是，关键类群发生了变化，从对照小鼠肠道中的有益菌属，如，，，转变为Vp感染小鼠中的机会致病菌，如，，，从而影响了小鼠体内与微生物群相关的生物学功能。具体而言，感染小鼠中与传染病和离子通道相关的通路显著增加，而与代谢、消化和细胞生长相关的通路则减少。我们认为，由于肠道微生物介导功能的改变，正常小鼠更容易受到Vp感染。所有这些影响都会降低肠道抵抗力，导致肠道黏膜严重受损，病原体泄漏到血液中，最终造成肝脏和肾脏损伤。这些发现极大地推进了我们对Vp、肠道微生物群和受感染宿主之间相互作用机制的理解。
