Probiotic Lactobacillus rhamnosus GG mono-association suppresses human rotavirus-induced autophagy in the gnotobiotic piglet intestine

Gut Pathogens

Jun Sun²  Xingdong Yang¹  Jacob Kocher¹  Ke Wen¹  Guohua Li¹  Fangning Liu¹  Yongguo Zhang²  Lijuan Yuan¹  Shaoping Wu² 

[1] Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Integrated Life Science Building, 1981 Kraft Dr, Blacksburg, VA 24061-0913, USA;Department of Biochemistry, Rush University, Cohn Research Building, 1735 W. Harrison Street, Chicago, IL 60612, USA

关键词: Rotavirus;    Probiotics;    Intestinal injury;    Intestinal inflammation;    Infectious disease;    Lactobacillus rhamnosus GG;    Gnotobiotic pig;    Diarrhea;    Apoptosis;    Autophagy;   

Others  :  821216
DOI  :  10.1186/1757-4749-5-22

 received in 2013-06-16, accepted in 2013-07-25,  发布年份 2013

【 摘 要 】

Background

Human rotavirus (HRV) is the most important cause of severe diarrhea in infants and young children. Probiotic Lactobacillus rhamnosus GG (LGG) reduces rotavirus infection and diarrhea. However, the molecular mechanisms of LGG-mediated protection from rotavirus infection are poorly understood. Autophagy plays an essential role in responses to microbial pathogens. However, the role of autophagy in HRV infection and LGG treatment is unknown. We hypothesize that rotavirus gastroenteritis activates autophagy and that LGG suppresses virus-induced autophagy and prevents intestinal damage in infected piglets.

Methods

We used LGG feeding to combat viral gastroenteritis in the gnotobiotic pig model of virulent HRV infection.

Results

We found that LGG feeding did not increase autophagy, whereas virus infection induced autophagy in the piglet intestine. Virus infection increased the protein levels of the autophagy markers ATG16L1 and Beclin-1 and the autophagy regulator mTOR. LGG treatment during viral gastroenteritis reduced autophagy marker expression to normal levels, induced apoptosis and partially prevented virus-induced tissue damage.

Conclusion

Our study provides new insights into virus-induced autophagy and LGG suppression of uncontrolled autophagy and intestinal injury. A better understanding of the antiviral activity of LGG will lead to novel therapeutic strategies for infant infectious diseases.

【 授权许可】

   
2013 Wu et al.; licensee BioMed Central Ltd.

【 图 表 】

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