Research Papers:

Lactobacillus reuteri ZJ617 maintains intestinal integrity via regulating tight junction, autophagy and apoptosis in mice challenged with lipopolysaccharide

Yanjun Cui, Li Liu, Xiaoxiao Dou, Chong Wang, Wenming Zhang, Kan Gao, Jianxin Liu and Haifeng Wang _

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Oncotarget. 2017; 8:77489-77499. https://doi.org/10.18632/oncotarget.20536

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Yanjun Cui1,2,*, Li Liu1,*, Xiaoxiao Dou1,*, Chong Wang1,*, Wenming Zhang1, Kan Gao1, Jianxin Liu2 and Haifeng Wang1,2

1Institute of Animal Nutrition, College of Animal Science and Technology, Zhejiang A & F University, Lin’an 311300, P.R. China

2College of Animal Science, MOE Key Laboratory of Molecular Animal Nutrition, Zhejiang University, Hangzhou 310029, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Haifeng Wang, email: [email protected]

Keywords: lactobacilli, intestinal barrier, apoptosis, autophagy, mice

Received: December 23, 2016    Accepted: July 30, 2017    Published: August 24, 2017


Live probiotics are effective in reducing gut permeability and inflammation. We have previously reported that Lactobacillus reuteri ZJ617 (ZJ617) with high adhesive and Lactobacillus rhamnosus GG (LGG) can ameliorate intestine inflammation induced by lipopolysaccharide (LPS). The present study was aimed at elucidating the roles of ZJ617 and LGG in alleviating the LPS-induced barrier dysfunction of ileum in mice. Six C57BL/6 mice per group were orally inoculated with ZJ617 or LGG for one week (1× 108 CFU/mouse) and intraperitoneally injected with LPS (10 mg/kg body weight) for 24 h. The results demonstrated that pretreatment with ZJ617 and LGG attenuated LPS-induced increase in intestinal permeability. The probiotics supplementation suppressed LPS-induced oxidative stress. Both ZJ617 and LGG strongly reversed the decline of occludin and claudin-3 expression induced by LPS challenge. ZJ617 relieved LPS-induced apoptosis by decreasing caspase-3 activity. Noticeably, ratio of microtubule-associated light chain 3 (LC3)-II/LC3-I and LC3 activity were elevated by LPS stimulation, whereas such increases were obviously attenuated by both of the probiotics treatment. Moreover, phosphorylated mammalian target of rapamycin (p-mTOR) was significantly inhibited by LPS, whereas complementation of ZJ617 and LGG markedly increased the expression of p-mTOR. Collectively, our results indicated that ZJ617 could protect LPS-induced intestinal barrier dysfunction via enhancing antioxidant activities and tight junction and attenuating apoptosis and autophagy via mTOR signaling pathway. These findings could serve as systematic mechanisms through which probiotics promote and maintain gut homeostasis.

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