Zhou Xiao-Yan, Li Ming, Li Xia, Long Xin, Zuo Xiu-Li, Hou Xiao-Hua, Cong Ying-Zi, Li Yan-Qing
Xiao-Yan Zhou, Ming Li, Xia Li, Xin Long, Xiu-Li Zuo, Yan-Qing Li, Department of Gastroenterology, Shandong University, Qilu Hospital, Jinan 250012, Shandong Province, China.
World J Gastroenterol. 2016 Jun 14;22(22):5211-27. doi: 10.3748/wjg.v22.i22.5211.
To evaluate gut microbial dysbiosis in two visceral hypersensitive models in comparison with irritable bowel syndrome (IBS) patients and to explore the extent to which these models capture the dysbiosis of IBS patients.
Visceral hypersensitivity was developed using the maternal separation (MS) rat model and post-inflammatory rat model. The visceral sensitivity of the model groups and control group was evaluated using the abdominal withdraw reflex score and electromyography in response to graded colorectal distention. The 16S ribosomal RNA gene from fecal samples was pyrosequenced and analyzed. The correlation between dysbiosis in the microbiota and visceral hypersensitivity was calculated. Positive findings were compared to sequencing data from a published human IBS cohort.
Dysbiosis triggered by neonatal maternal separation was lasting but not static. Both MS and post-inflammatory rat fecal microbiota deviated from that of the control rats to an extent that was larger than the co-housing effect. Two short chain fatty acid producing genera, Fusobacterium and Clostridium XI, were shared by the human IBS cohort and by the maternal separation rats and post-inflammatory rats, respectively, to different extents. Fusobacterium was significantly increased in the MS group, and its abundance positively correlated with the degree of visceral hypersensitivity. Porphyromonadaceae was a protective biomarker for both the rat control group and healthy human controls.
The dysbiosis MS rat model and the post-inflammatory rat model captured some of the dysbiosis features of IBS patients. Fusobacterium, Clostridium XI and Porphyromonadaceae were identified as targets for future mechanistic research.
与肠易激综合征（IBS）患者相比，评估两种内脏高敏模型中的肠道微生物失调情况，并探讨这些模型在多大程度上反映了IBS患者的失调情况。
采用母婴分离（MS）大鼠模型和炎症后大鼠模型建立内脏高敏状态。使用腹部撤回反射评分和肌电图对模型组和对照组在分级结肠扩张刺激下的内脏敏感性进行评估。对粪便样本中的16S核糖体RNA基因进行焦磷酸测序和分析。计算微生物群失调与内脏高敏之间的相关性。将阳性结果与已发表的人类IBS队列的测序数据进行比较。
新生儿母婴分离引发的微生物失调是持续的，但并非一成不变。MS大鼠和炎症后大鼠的粪便微生物群与对照大鼠相比均有偏离，且偏离程度大于同笼饲养的影响。人类IBS队列与母婴分离大鼠和炎症后大鼠分别不同程度地共有两个产生短链脂肪酸的菌属，即梭杆菌属和XI群梭菌属。梭杆菌属在MS组中显著增加，其丰度与内脏高敏程度呈正相关。卟啉单胞菌科对大鼠对照组和健康人类对照组均为保护性生物标志物。
MS大鼠模型和炎症后大鼠模型捕捉到了IBS患者的一些微生物失调特征。梭杆菌属、XI群梭菌属和卟啉单胞菌科被确定为未来机制研究的靶点。
