Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis (Hepatology, 2007, 46:841-850)

報告日期: 2007/10/16
報告時間: 17:10/18:00
報告學生: 蔡政潔
講評老師: 黎煥耀
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Probiotic Bacteria Prevent Hepatic Damage and Maintain Colonic Barrier Function in a Mouse Model of Sepsis

Ewaschuk, J. et al. Hepatology, 46, 841-501 (2007)

Student: Cheng-Chieh Tsai (蔡政潔)

Commentator: Dr. Huan-Yao Lei (黎煥耀 博士)

Time: 17:10-18:00, Oct. 16, 2007

Place: Room 602

 

Abstract

Sepsis, excessive tumor necrosis factor alpha (TNF-a) that induces a breakdown of intestinal barrier function and allows the translocation of bacteria to the liver has shown to play a key role in the pathogenesis of liver failure1. Probiotics are live microorganisms which beneficially affect the host by improving the intestinal microflora balance. Recent studies indicated that probiotic bacteria may be used to treat the disturbed intestinal microflora and the intestinal barrier dysfunction2. Result showed that the expression of peroxisome proliferator-activated receptor gamma (PPARg) was higher in the colon and liver than other organ. Thus, the activation of the PPARg receptor had potent anti-inflammatory functions through attenuating the onset and severity of septic shock by modulating nuclear factor kappa B (NF-kB) activity3. In this study, the authors investigated the therapeutic effects of probiotic bacteria in attenuating hepatic and intestinal injury induced by lipopolysaccharide (LPS) and D-galactosamine (GalN) in a mouse model. They found that treating LPS/GalN induced a significant increase of proinflammatory cytokines secretion, disrupted colonic barrier function, bacterial translocation, and severe hepatic injury in mice. However, oral administration of probiotics can reduce liver damage, bacterial translocation, secretion of the proinflammatory cytokines, and maintained gut barrier function effectively. Besides, the probiotic pretreatment prevented the reduction in hepatic, but not colonic, protein PPARg and its target gene lipocalin-2 expression in LPS/GalN-treated mice. A selective PPARg antagonist, GW9662, abrogated the protective effects of probiotics after LPS/GalD challenge. Taken together, the probiotics effectively protect liver and intestinal damage via PPARg-dependent mechanism in a mouse model of sepsis.

 

References

1.      Hassoun, H. T. et al. 2001. Post-injury multiple organ failure: the role of the gut. Shock 15: 1-10.

2.      O'Sullivan, G. C. et al. 2005. Probiotics: an emerging therapy. Curr. Pharm. Des. 11: 3-10.

3.      Dubuquoy, L. et al. 2002. Role of peroxisome proliferator-activated receptor gamma and retinoid X receptor heterodimer in hepatogastroenterological diseases. Lancet 360: 1410-1418.