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

Wu S, Yuan L, Zhang Y, Liu F, Li G, Wen K, Kocher J, Yang X, Sun J - Gut Pathog (2013)

Bottom Line: We found that LGG feeding did not increase autophagy, whereas virus infection induced autophagy in the piglet intestine.LGG treatment during viral gastroenteritis reduced autophagy marker expression to normal levels, induced apoptosis and partially prevented virus-induced tissue damage.A better understanding of the antiviral activity of LGG will lead to novel therapeutic strategies for infant infectious diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, Rush University, Cohn Research Building, 1735 W, Harrison Street, Chicago, IL 60612, USA. jun_sun@rush.edu.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

LGG inhibits autophagy proteins enhanced by HRV in Gn pig ileum. Autophagy proteins in pig ileum treated with LGG and HRV. Ileum epithelia were scraped on PID 2. Relative protein band intensities of ATG16L1 in pig ileum were analyzed with NIH image. Data are reported as the mean ± SD. ANOVA, * P<0.05.
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Figure 2: LGG inhibits autophagy proteins enhanced by HRV in Gn pig ileum. Autophagy proteins in pig ileum treated with LGG and HRV. Ileum epithelia were scraped on PID 2. Relative protein band intensities of ATG16L1 in pig ileum were analyzed with NIH image. Data are reported as the mean ± SD. ANOVA, * P<0.05.

Mentions: To determine the effects of probiotic LGG on autophagy-related proteins, we immunoblotted for p-mTOR, mTOR, VPS34, ATG16L1, and Beclin-1 in small intestinal epithelial cells (Figure 2). LGG inhibited the expression of p-mTOR, mTOR, VPS34, Beclin-1 and ATG16L1, which were otherwise elevated by HRV infection (Figure 2).


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

Wu S, Yuan L, Zhang Y, Liu F, Li G, Wen K, Kocher J, Yang X, Sun J - Gut Pathog (2013)

LGG inhibits autophagy proteins enhanced by HRV in Gn pig ileum. Autophagy proteins in pig ileum treated with LGG and HRV. Ileum epithelia were scraped on PID 2. Relative protein band intensities of ATG16L1 in pig ileum were analyzed with NIH image. Data are reported as the mean ± SD. ANOVA, * P<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750464&req=5

Figure 2: LGG inhibits autophagy proteins enhanced by HRV in Gn pig ileum. Autophagy proteins in pig ileum treated with LGG and HRV. Ileum epithelia were scraped on PID 2. Relative protein band intensities of ATG16L1 in pig ileum were analyzed with NIH image. Data are reported as the mean ± SD. ANOVA, * P<0.05.
Mentions: To determine the effects of probiotic LGG on autophagy-related proteins, we immunoblotted for p-mTOR, mTOR, VPS34, ATG16L1, and Beclin-1 in small intestinal epithelial cells (Figure 2). LGG inhibited the expression of p-mTOR, mTOR, VPS34, Beclin-1 and ATG16L1, which were otherwise elevated by HRV infection (Figure 2).

Bottom Line: We found that LGG feeding did not increase autophagy, whereas virus infection induced autophagy in the piglet intestine.LGG treatment during viral gastroenteritis reduced autophagy marker expression to normal levels, induced apoptosis and partially prevented virus-induced tissue damage.A better understanding of the antiviral activity of LGG will lead to novel therapeutic strategies for infant infectious diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biochemistry, Rush University, Cohn Research Building, 1735 W, Harrison Street, Chicago, IL 60612, USA. jun_sun@rush.edu.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus