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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 | CCL17-expressingT cell homeostasis in mice显示文摘 | Weber C Meiler S Doring Y | 2011 | J Clin Invest2011，121，7： | 1 |
| 3 | CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice显示文摘 | Weber C Meiler S Dring Y | 2011 | J Clin Invest2011，121，7： | 1 |
| 4 | CCL17-expressing dendritic ceils drive atherosclerosis by restraining regulatory T cell homeostasis in mice 显示文摘 | Weber C Meiler S Dsring Y | 2011 | J Clin Invest2011，121，： | 1 |
| 5 | 18 F-FDG PET and PET/CT in fever of unknown origin显示文摘 | MEILER J SAHLMANN C O SCHEEL A K | 2007 | J Nucl Med2007，48，1： | 1 |
| 6 | CCL17 - expressing dendritic ceils drive atherosclerosis by restraining regulatory T cell homeostasis in mice显示文摘 | Weber C Meiler S Doring Y | 2011 | J Clin Invest2011，121，17： | 1 |
| 7 | CCL17-expressing dendriticcells drive atherosclerosis by restraining regulatory T cell homeostasisin mice显示文摘 | Weber C Meiler S Koch M | 2011 | J Clin Invest2011，121，7： | 1 |
| 8 | CCLl7-expressing dendritic cells drive atheroscleresis by restraining regulatory T cell homeostasis in mice显示文摘 | Weber C Meiler S Doring Y | 2011 | J Clin Invest2011，121，7： | 1 |
| 9 | CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice显示文摘 | Weber C Meiler S Doring Y | 2011 | J Clin Invest2011，121，7： | 1 |
| 10 | Dipolar couplings in multiple alignments suggest alpha helical motion in ubiquitin显示文摘 | Meiler J Peti W Griesinger C | 2003 | J Am Chem Soc2003，125，27： | 1 |
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