抗生素改变肠道菌群,可导致神经炎症和焦虑
  • 口服氨苄青霉素使小鼠产生焦虑样行为和结肠炎,肠道中变形菌门(尤其是产酸克雷伯氏菌)增加、乳酸杆菌减少,血液LPS增多;
  • 将上述小鼠粪菌、产酸克雷伯菌或这种菌的LPS(KL),移植给其它小鼠,也可诱导焦虑和结肠炎,增加海马内的免疫细胞募集和脑内凋亡的神经元;
  • 氨苄青霉素、产酸克雷伯菌和KL可诱导结肠和大脑炎症,促进NF-κB活化、IL-1β和TNF-α表达,并增加肠道通透性;
  • 口服罗伊氏乳杆菌可缓解抗生素诱导的焦虑和结肠炎。
主编推荐语
mildbreeze
Mucosal Immunology[IF:7.478]近期发表一项小鼠研究,表明口服抗生素氨苄青霉素可导致小鼠肠道菌群改变,使小鼠产生结肠和神经炎症,以及焦虑样行为。并鉴定出产酸克雷伯氏菌或许是“元凶”之一,而口服罗伊氏乳杆菌可缓解抗生素造成的焦虑和炎症。该研究有助于加深对肠脑轴——特别是肠道菌群、炎症和行为间的关联——的理解,相关发现是否适用于人体还需进一步验证。
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Mucosal Immunology [IF:6.726]

Evidence for interplay among antibacterial-induced gut microbiota disturbance, neuro-inflammation, and anxiety in mice

小鼠中抗菌药诱导的肠道菌群扰动、神经炎症和焦虑之间相互作用的证据

10.1038/s41385-018-0042-3

2018-06-04, Article

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The aim of the present study was to determine whether there is the mechanistic connection between antibacterial-dependent gut microbiota disturbance and anxiety. First, exposure of mice to ampicillin caused anxiety and colitis and increased the population of Proteobacteria, particularly Klebsiella oxytoca, in gut microbiota and fecal and blood lipopolysaccharide levels, while decreasing lactobacilli population including Lactobacillus reuteri. Next, treatments with fecal microbiota of ampicillin-treated mouse (FAP), K. oxytoca, or lipopolysaccharide isolated from K. oxytoca (KL) induced anxiety and colitis in mice and increased blood corticosterone, IL-6, and lipopolysaccharide levels. Moreover, these treatments also increased the recruitment of microglia (Iba1+), monocytes (CD11b+/CD45+), and dendritic cells (CD11b+/CD11c+) to the hippocampus, as well as the population of apoptotic neuron cells (caspase-3+/NeuN+) in the brain. Furthermore, ampicillin, K. oxytoca, and KL induced NF-κB activation and IL-1β and TNF-α expression in the colon and brain as well as increased gut membrane permeability. Finally, oral administration of L. reuteri alleviated ampicillin-induced anxiety and colitis. These results suggest that ampicillin exposure can cause anxiety through neuro-inflammation which can be induced by monocyte/macrophage-activated gastrointestinal inflammation and elevated Proteobacteria population including K. oxytoca, while treatment with lactobacilli suppresses it.

First Authors:
Hyo-Min Jang,Hae-Ji Lee

Correspondence Authors:
Dong-Hyun Kim

All Authors:
Hyo-Min Jang,Hae-Ji Lee,Se-Eun Jang,Myung Joo Han,Dong-Hyun Kim

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