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| 1 | Different effects of a CD14 gene polymorphism on disease outcome in patients with alcoholic liver disease and chronic hepatitis C infection显示文摘AIM: Clinical and experimental data suggest that gut-derived endotoxins are an important pathogenic factors for progression of chronic liver disease. Recently, a C-T (-159)polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression and to be associated with advanced alcoholic liver damage. Here, we investigated this polymorphism in patients with less advanced alcoholic liver disease (ALD)and chronic hepatitis C virus (HCV) infection.METHODS: CD14 genotyping was performed by PCR-RFLP analysis in (a) 121 HCV patients, (b) 62 patients with alcohol-associated cirrhosis (Alc-Ci), (c) 118 individuals with heavy alcohol abuse without evidence of advanced liver damage (Alc-w/o Ci), and (d) 247 healthy controls.Furthermore, serum levels of soluble CD14 (sCD14) and transaminases were determined.RESULTS: The TT genotype was significantly more frequent in Alc-Ci compared to Alc-w/o Ci or controls (40.3% vs 23.7% or 24.0%, respectively). In Alc-w/o Ci,serum levels of transaminases did not differ significantly between patients with different CD14 genotypes. In HCV patients, TT-homozygotes had significantly higher sCD14 levels and sCD14 serum levels were significantly higher in patients with advanced fibrosis or cirrhosis. However,no association was found between CD14 genotypes and histological staging or grading.CONCLUSION: Considering serum transaminases as surrogate markers for alcoholic liver damage, the CD14 polymorphism seems to exhibit different effects during the course of ALD. Differences in genotype distribution between cirrhotic HCV patients and alcoholics and the known functional impact of this polymorphism on CD14 expression levels further indicate differences in the pathophysiological role of CD14 and CD14-mediated lipopolysaccharides signal transduction with regard to the stage as well as the type of the underlying liver disease. | C Meiler M Mühlbauer M Johann A Hartmann B Schnabl N Wodarz G Schmitz J Schlmerich C Hellerbrand | 2005 | World Journal of Gastroenterology2005，11，38： | 3 |
| 2 | Role of innate immunity and the microbiota in liver fibrosis: crosstalk between the liver and gut 显示文摘 | Seki E Schnabl B | 2012 | J Physiol2012，590，3： | 1 |
| 3 | Gangliosides protect bowel in an infant model of necrotizing enterocolitis by suppressing proinflammatory signals 显示文摘 | Schnabl KL Larsen B Van Aerde JE | 2009 | J Pediatr Gas- troenterol Nutr2009，49，4： | 1 |
| 4 | CD40 activates NFkappaB and c-Jun N-terminal kinase and enhances chemokine secretion onactivated human hepatic stellate cells 显示文摘 | Schwabe RF Schnabl B Kweon YO | 2001 | Immunol2001，166，11： | 1 |
| 5 | Role of innate immunity and the microbiota in liver fibrosis:crosstalk between the liver and gut显示文摘 | Seki E Schnabl B | 2012 | Physiol2012，590，3： | 1 |
| 6 | The role of S mad3 in mediating mouse hepatic stellate cell activation显示文摘 | Schnabl B Kweon YO Frederick JP | 2001 | Hepatology2001，34，1： | 1 |
| 7 | The role of Smad3 in mediating mouse hepatic stellate cell activation显示文摘 | Schnabl B Kweon YO Frederick JP | 2001 | Hepatology2001，34，1： | 1 |
| 8 | Dexrazoxane (ICRF-187) protects cardiac myocytes against doxorubicin by preventing damage to mitochondria显示文摘 | HASINOFF B B SCHNABL K L MARUSAK R A | 2003 | Cardiovascular Toxicology2003，3，2： | 1 |
| 9 | The role of Smad3 in mediating mouse hepatic stellate cell activation显示文摘 | Kweon Yo Frederick Jp | 2001 | Hepatology2001，34，1： | 1 |
| 10 | The role of Smad3 in mediating mouse hepatic stellate cell activation显示文摘 | Schnabl B Kweon YO Frederick JP | 2001 | Hepatology2001，34，： | 1 |
| 11 | The role of Smad3 in mediating mouse hepatic stellate cell activation 显示文摘 | Schnabl B Kweon YO Frederick JP | 2001 | Hepatology2001，34，1： | 1 |
| 12 | Zinc finger protein 267 is up-regulated during the activation process of human hepatic stellate cells and functions as a negative transcriptional regulator of MMP-10显示文摘 | Schnabl B Hu K Muhlbauer | 2005 | Biochem Biophys Res Commun2005，335，1： | 1 |
| 13 | TAKI/JNK and p38 have opposite eaffeets on rat hepatic stellate cells 显示文摘 | Schnabl B Bradham CA Bennett BL | 2001 | Hepatology2001，34，5： | 1 |
| 14 | CD40 actives NF-kappa B and c-jun N-terminal kinase and enchances chemokine secretion on actived human hepatic stellate cells显示文摘 | Schwabe RF Schnabl B Kweon YO | 2001 | J Immunol2001，166，11： | 1 |
| 15 | TAK1/JNK and p38 have opposite effects on rat hepatic stellate cells显示文摘 | Schnabl B Bradham CA Bennett BL | 2001 | J Hepatol2001，34，5： | 1 |
| 16 | Interactions Between The Intestinal Microbiome AndLiver Diseases 显示文摘 | Schnabl B Brenner D A | 2014 | Gastroenterology2014，146，6： | 1 |
| 17 | The role of Smad3 in mediating mouse hepatic stellate cell activation 显示文摘 | Schnabl B Kweon Yo Frederick Jp | 2001 | Hepatology2001，34，1： | 1 |
| 18 | Linking Intestinal Homeostasis And Liver Disease 显示文摘 | Schnabl B | 2013 | Current OpinionIn Gastroenterology2013，29，3： | 1 |
| 19 | TAK1/JNK and p38 have opposite effects on rat hepatic stellate cells显示文摘 | Schnabl B Bradham C A Bennett B L | 2001 | Hepatology2001，34，5： | 1 |
| 20 | Cangliosides protectbowel in an infant model of necrotizing enterocolitis bysuppressing proinflammatory signals 显示文摘 | Schnabl KL Larsen B Van Aerde JE | 2010 | Pediatr GastroenterolNutr2010，51，5： | 1 |
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