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Expression of TLR3 and TLR4 on Hepatocytes in Patients with Chronic Hepatitis B and Its Clinical Significance

Author: LiBing
Tutor: GongGuoZhong
School: Central South University
Course: Inner science of infectious diseases
Keywords: TLR3 TLR4 CHB Correlation Immunohistochemistry
CLC: R512.62
Type: Master's thesis
Year: 2011
Downloads: 72
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Abstract

The pathogenesis of chronic hepatitis B (Chronic Hepatitis B, CHB) has been the focus of research in the field of infectious diseases and difficult. So far, the hepatitis B virus (JOURNAL B Virus HBV) infection chronic persistent infection mechanism has not been elucidated. In the case of CHB treatment of the lack of effective measures, the study of HBV infection, chronic and persistent infection mechanism is particularly important and urgent. Chronic HBV infection should be the result of natural immune (innate immune) and adaptive immunity together, HBV mechanism of chronic infection, innate immunity may play a more important role. Natural immune molecules in the Toll-like receptors (Toll like receptors, TLRs) are mainly distributed in the immune cells, especially the non-specific immune cells, as well as certain somatic cell surface, not only the activation of the innate immune response, causing the release of cytokines, in the natural immune and inflammatory response in a central hub role, and provide the necessary startup Acquired Immune activation signal to initiate apoptosis, signal transduction. DsRNA generated wherein TLR3 can identify presence in the viral genome or virus replication, the start signal transduction pathway induced nuclear transcription factor KB (nuclear factor-KB, of NF-kappaB) of the indexable and [FN-of β expression; of TLR4 identification leather Lan Gram negative bacteria cell wall outer endotoxin the main ingredient lipopolysaccharide (lipopolysaccharides, LPS) to start the activation of the signal transduction pathway for induction of NF-κB and protein kinase -1 (activator protein 1, AP-1). Liver parenchymal cells and non-parenchymal cells express TLR3 and TLR4, TLR3 and TLR4 signaling system in the development of the disease in the liver may play an important role. Research TLR3 and TLR4 expression in liver cells in CHB patients and their signal transduction pathways useful in understanding the chronic HBV infection and CHB pathogenesis. Purpose of this subject by detection CHB patients with liver tissue TLR3, TLR4 expression changes and liver pathological lesions (inflammatory activity of liver tissue, liver tissue fibrosis stage), CHB clinical, serum HBV DNA load the level of serum HBV-HBeAg state relations, and to explore the relevance of TLR3, TLR4 and CHB TLR3 role in the pathogenesis of CHB of TLR4 and TLR3, of TLR4 For the clinical significance of CHB. Research methods 1.140 cases of CHB liver tissue biopsy immunohistochemical SABC staining TLR3, TLR4 expression and ratings. Liver histopathology by hematoxylin and eosin (HE), argyrophilic reticular fibers dyed. Then liver tissue TLR3, TLR4 expression score and liver pathological inflammatory activity and fibrosis stage, clinical grading and the level of serum HBV DNA level, serum HBV-HBeAg correlation analysis. Results 1.TLR3 expressed in CHB patients with liver tissue is weak, mainly expressed in the cytoplasm of liver cells, expression in the nucleus, the cell membrane without staining; TLR4 expressed mainly in the cytoplasm of liver cells in CHB patients with liver tissue, some liver cell membrane expression, no expression in the nucleus. 2. Liver tissue TLR3 expression level of strength and CHB patients with serum HBV DNA level, serum HBV-HBeAg status, clinical grading liver tissue inflammation grades (G), the degree of liver fibrosis staging (S There was no significant relationship (P gt; 0.05)) between. 3.TLR4 expression intensity in light, moderate and severe CHB patients with liver tissue differences was statistically significant (H = 16.59, P lt; 0.05), Spearman rank correlation analysis of the liver tissue of TLR4 immunohistochemistry staining intensity strength CHB clinical degree was a positive correlation (rs = 0.339, P lt; 0.05), the linear trend test showed that TLR4 expression intensity with CHB clinical indexing linear relationship (P lt; 0.05) Description the TLR4 expression strength CHB clinical indexing between correlation exists not only for the linear relationship between intensity and increased with the increase of CHB clinical, TLR4 expression. Related to the degree of inflammatory activity 4.TLR4 expression CHB patients with liver histological. G1-G4 four groups of liver tissue between TLR4 expression intensity difference was statistically significant (P lt; 0.05), Spearman rank correlation analysis showed that TLR4 expression intensity of liver inflammation grading (G) was positively correlated (rs = 0.574, P lt; 0.05), the linear trend test showed that TLR4 expression intensity of liver tissue inflammation grades (G) there is a linear relationship (P = lt; 0.05), TLR4 expression intensity and liver inflammation activity of correlation exists not only between the grade (G) is a linear relationship between intensity and increased with increasing liver inflammation grading (G), TLR4 expression. 5.TLR4 expression CHB patients with liver tissue fibrosis. S1-S4 CHB patients in the stage of fibrosis, liver tissue between the four groups of TLR4 expression intensity difference had statistical significance (P lt; 0.05), Spearman rank correlation analysis showed that TLR4 expression intensity and degree of liver fibrosis in phase (S) were positively correlated (rs = 0.485, P lt; 0.05), a linear trend test TLR4 expression intensity of liver tissue fibrosis staging (S) there is a linear relationship (P lt; 0.05) Description TLR4 expression correlation exists not only between the intensity of the liver tissue fibrosis stage (S)) and a linear relationship, TLR4 expression intensity and increased with the degree of liver fibrosis staging (S)) increase. Liver tissue TLR4 expression level of strength and CHB patients with serum HBV DNA load serum HBV-HBeAg status were not correlated (P gt; 0.05). TLR4 expression in the liver tissue on Conclusion 1.CHB patients enhanced activity of liver tissue inflammation, fibrosis and the severity of the disease, and the level of serum HBV DNA load, regardless of the status of serum HBV-HBeAg, TLR4 may be involved in CHB's pathogenesis, most likely CHB immune injury. TLR3 expression is weak in the on 2.CHB liver tissue in patients with liver tissue inflammation activity, fibrosis and the severity of the disease and the level of serum HBV DNA load, regardless of the status of serum HBV-HBeAg. The the TLR3 expression without markedly enhanced HBV-infected liver cells did not to activate TLR3 expression, suggesting that its antiviral mechanism induced cell not play, it may also lead to the body's immune clearance of HBV infection ability decline may HBV one of the reasons why chronic infection.

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