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The Mechanism Research On The CD14,TLR4 Gene Expression And Inflammatory Cytokines In Endotoxin Induced The Severity Of Hepatitis

Posted on:2007-11-11Degree:MasterType:Thesis
Country:ChinaCandidate:X Y ChengFull Text:PDF
GTID:2144360212956583Subject:Internal Medicine
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[Background and Aims] Intestinal endotoxemia(IETM) plays the key role in the development of severity of viral hepatitis B. At persent it is considered that IETM could induce systemic inflammatory response syndrome by activating the system of mononuclear macrophages and a great quantity proinflammatory cytokines, such as TNFα,IL-1β,and IL-6 were released ,which could result in much more damage of hepatocytes and evenmore the live failure .It has not been reported that how the endotoxin activated the systemic inflammatory response syndrome and what role the endotoxin receptor on the mononuclear macrophages and the expression of induced downstream introcellular signaling molecular played in chronic severe hepatitis B. Our experiment was trying to explain the mechanism of the severity of hepatitis by the core signal conduction pathway of CD 14 and TLR4,and by the induceded systemic inflammatory response syndrome. At the same time , the relativity between the CD14 and the proinflammatory factors of TNFα had be further exploited. [Methods] The expression of membrane CD 14, CD14mRNA and TLR4mRNA in the peripheral blood mononuclear cells (PBMCs) from 40 cases of chronic severe hepatitis patients B, 20 cases of chronic hepatitis B patients and 20 cases of healthy controls were detected by flow cytometry and reverse transcription-polymerase reaction (RT-PCR) methods respectively. Moreover, the level of endotoxin were assayed by limulus amebocyte lysate test and the level of TNFα, IL-1β, IL-6 were detected by Enzyme-linked immunoadsordent Assay(ELISA). [Results] The expression of mCD14 in PBMCs were significantly higher in chronic severe hepatitis patients (74.23 ±12.28 ) than those in chronic hepatitis patients (63.62...
Keywords/Search Tags:chronic severe, hepatitisB, endotoxemia, CD14, inflammatory cytokines
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