Yao Guoqiang, Cao Chenxia, Zhang Meng, Kwok Lai-Yu, Zhang Heping, Zhang Wenyi
Key Laboratory of Dairy Biotechnology and Engineering, Ministry of Education, Inner Mongolia Agricultural University, Hohhot, People's Republic of China.
Key Laboratory of Dairy Products Processing, Ministry of Agriculture and Rural Affairs, Inner Mongolia Agricultural University, Hohhot, People's Republic of China.
Comput Struct Biotechnol J. 2021 Oct 22;19:5888-5897. doi: 10.1016/j.csbj.2021.10.026. eCollection 2021.
Probiotics administration can facilitate the restoration of host gut microbiota/metabolome after antibiotic treatment. Yet, the mechanism behind such beneficial effects remains unclear. This study constructed a rat model of antibiotic-induced gut dysbiosis to monitor the effects and mechanism of probiotic ( Zhang) treatment in maintaining gut homeostasis and restoring the gut microbiota/metabolome. Forty rats were randomly divided into four groups (n = 10 per group): control receiving only saline (Ctrl), antibiotic (AB-Ctrl), antibiotic followed by probiotic (AB-Prob), and antibiotic plus probiotic followed by probiotic (AB + Prob). Rat fecal microbiota and sera were collected at four time points from pre-treatment to post-treatment. The probiotic-treated group (AB + Prob) had significantly more (.) after one week of antibiotic and probiotic intervention but fewer antibiotic resistance genes (ARGs)-possessing bacteria ( and bacterium). Consistently, metabolomics data revealed that both probiotic groups had more acetic acid, propionic acid, butyric acid, and valeric acid post treatment. Moreover, a potential probiotic species, , strongly correlated with , as well as propionic acid, butyric acid, and valeric acid. Furthermore, administering probiotic lowered the serum IL-1α level. In contrast, the antibiotic-recipients had a higher irreversible level of IL-1α, suggesting inflammation of the rats. Thus, antibiotic treatment not only led to host gut dysbiosis, but inflammatory responses and an increase in gut ARGs. Daily Zhang supplementation could alleviate the side effect of cefdinir intervention and facilitate the restoration of gut microbial homeostasis, and these probiotic effects might involve -mediated beneficial activities.
施用益生菌可促进抗生素治疗后宿主肠道微生物群/代谢组的恢复。然而，这种有益作用背后的机制仍不清楚。本研究构建了抗生素诱导的肠道菌群失调大鼠模型，以监测益生菌（张）治疗在维持肠道稳态和恢复肠道微生物群/代谢组方面的效果和机制。40只大鼠随机分为四组（每组n = 10）：仅接受生理盐水的对照组（Ctrl）、抗生素组（AB-Ctrl）、抗生素后接益生菌组（AB-Prob）以及抗生素加益生菌后再接益生菌组（AB + Prob）。在从预处理到治疗后的四个时间点收集大鼠粪便微生物群和血清。在抗生素和益生菌干预一周后，益生菌治疗组（AB + Prob）的（.）明显更多，但具有抗生素抗性基因（ARGs）的细菌（和细菌）更少。一致地，代谢组学数据显示，两个益生菌组在治疗后乙酸、丙酸、丁酸和戊酸更多。此外，一种潜在的益生菌物种与以及丙酸、丁酸和戊酸密切相关。此外，施用益生菌可降低血清IL-1α水平。相比之下，接受抗生素的大鼠IL-1α水平不可逆地更高，表明大鼠存在炎症。因此，抗生素治疗不仅导致宿主肠道菌群失调，还引发炎症反应并增加肠道ARGs。每日补充张可减轻头孢地尼干预的副作用并促进肠道微生物稳态的恢复，这些益生菌作用可能涉及介导的有益活动。
