Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remains unclear. It has been proposed that a direct viropathic effect, the host immune response, or both mediate cell damage. To address this issue, the immunophenotype of the inflammatory infiltrate in the liver of 18 patients with abnormal liver function tests and serologically detectable hepatitis C virus antibodies was compared with seven control patients (three cases with hepatitis B virus infection, two with alcoholic hepatitis, and one patient each with primary biliary cirrhosis and autoimmune hepatitis). The immunohistochemical markers included UCHL1, L26, Ham-56, Mac-387, CD68, Leu-M1, and cathepsin B. We found that T cells represent the predominant cell type in both histopathologic patterns of hepatitis C, ie, chronic active hepatitis and chronic persistent hepatitis, but the intensity of the T-cell infiltrate displayed marked differences. B-cell infiltrates were only seen in the germinal centers of lymphoid follicles in portal tracts. Furthermore, significant numbers of CD68-positive macrophages/monocytes were seen in the more aggressive form of hepatitis C viral infection. These data suggest that the T-lymphocyte-mediated host immune response is similar in chronic active and chronic persistent hepatitis patterns of hepatitis C viral infection, but varies in its intensity. In addition, macrophages/monocytes may play a role in hepatocyte and bile duct injury in chronic hepatitis C.
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PMID:Chronic hepatitis C. Analysis of host immune response by immunohistochemistry. 753 56

Liver macrophages, which are involved in the different types of hepatitis, may indirectly induce hepatic fibrogenesis, since they have the possibility to activate hepatic stellate cells and fibroblasts by secretion of TGF-beta, TNF-alpha and IL-1. To evaluate variations of the number of liver macrophages and their subpopulations, a quantification was carried out in normal human liver tissue, fatty liver, fatty liver hepatitis and hepatitis B. Identification was performed by the mab PG-M1 (anti-CD68) and, comparatively, four lectins, Griffonia simplicifolia agglutinin I (GSA-I), Erythrina cristagalli agglutinin (ECA), peanut agglutinin (PNA) and soybean agglutinin (SBA). A slight decrease in the frequency of macrophages in pericentral fields was observable in fatty liver and fatty liver hepatitis as compared to normal liver tissue. On the other hand, the number of CD68+ cells was significantly enhanced in hepatitis B with moderate and severe inflammatory activity. The highest incidence of macrophages was found in portal tracts of liver with fatty liver hepatitis and, particularly, hepatitis B. The fraction of cells stained by ECA, PNA or SBA did not increase significantly under pathological conditions. In contrast, the percentage of GSA-I binding macrophages was higher in liver parenchyma of hepatitis B and in portal tract macrophages in fatty liver hepatitis and also hepatitis B. In conclusion, our results indicate that GSA-I may aid in the detection of the subpopulation of activated macrophages which are assumed to play a pivotal role in liver pathology.
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PMID:Comparative quantitative analysis of macrophage populations defined by CD68 and carbohydrate antigens in normal and pathologically altered human liver tissue. 969 43

A 57-year-old man presented with jaundice. Abdominal computed tomography showed a 10-cm left hepatic lobe heterogeneous solid mass with low attenuated areas in the mass, multiple liver metastases and lung metastasis. Serology for hepatitis B and C were negative. Serum alpha-fetoprotein, CEA and CA19-9 were normal. The patient died a few weeks later of progressive liver failure and an autopsy was performed. Histologically, the tumor consisted of sarcomatoid mononuclear cells and osteoclast-like giant cells. The liver tissue surrounding the tumor showed no cirrhotic pattern. The osteoclast-like giant cells were uniformly and strongly immunoreactive with CD68. The mononuclear cells demonstrated expression of vimentin but were negative for CAM5.2. The MIB-1 index was 20% for the mononuclear cells. In conclusion, the histopathological diagnosis revealed an osteoclast-like giant cell tumor of the liver.
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PMID:[Osteoclast-like giant cell tumor (OGCT) of the liver: report of a case]. 2230 49

Hepatitis B virus (HBV) infection is a major public health problem, and HBV-related acute-on-chronic liver failure (HBV-ACLF) has an extremely poor prognosis due to a lack of understanding of pathogenesis as well as a lack of effective treatments. Signals from the inhibitory receptor programmed death-1 (PD-1) have been demonstrated to be involved in regulating the pathogenesis of infectious diseases. However, the expression of PD-1 and its ligands in HBV-ACLF patients has yet to be evaluated. In this study, the expression of PD-1 and its ligands, PD-L1 and PD-L2, in liver biopsies from HBV-ACLF as well as chronic hepatitis B (CHB) patients were analyzed by immunohistochemistry. The results showed that all three molecules were observed in the HBV-ACLF samples and their levels were significantly higher than they were in CHB. Immunofluorescence double-staining showed that PD-1 was found on CD3(+), CD8(+) T cells, CD56(+) NK cells, CD68(+) macrophages, CK-18(+) epithelial cells, and CD16(+) monocytes. The PD-L1 expression was observed on all cell types detected and the PD-L2 was chiefly on CK-18(+) epithelial cells and CD31(+) endothelial cells. Interestingly, high levels of virus-induced procoagulant molecule fibrinogen-like protein 2 (FGL2) were observed in liver sections from HBV-ACLF, and PD-L1 and PD-L2 expression was also observed on FGL2(+) cells in these patients. Our combined results suggest that the expression of PD-L1 and PD-L2 may be biomarkers to identify and diagnose ACLF, and a clear understanding of their functional roles should further elucidate the pathogenesis of this disease.
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PMID:Intrahepatic expression of programmed death-1 and its ligands in patients with HBV-related acute-on-chronic liver failure. 2289 98

We report a unique case of multicentric reticulohistiocytosis (MRH) associated with liver carcinoma. A 61-year-old man presented with a 4-month history of nonpruritic, generalized, ruby-red papules and nodules, accompanied by fever, joint swelling and difficulty in swallowing. Skin histology showed polymorphic histiocyte infiltration with typical 'ground glass' cytoplasm. Further immunohistochemical studies characterized the lesions as positive for leukocyte common antigen, HLA-DR and CD68. The patient had a history of hepatitis B, and systemic examination, including carcinoma index and type-B ultrasonic examination, revealed high levels of AFP and a solid tumor, which was considered malignant, localized on the right lobe of the liver. Treatment of the liver carcinoma resulted in a significant improvement of the skin symptoms. This is the first case study to report an association between MRH and liver carcinoma. A review of the English-language literature reveals the close linkage between MRH and malignancy. All patients with MRH should be evaluated and monitored carefully to determine the underlying neoplasm.
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PMID:Multicentric reticulohistiocytosis associated with liver carcinoma: report of a case. 2294 98

Hepatitis B virus (HBV) is a major public health problem, and HBV-related acute-on-chronic liver failure (HBV-ACLF) has an extremely poor prognosis due to a lack of effective treatments. B7-H3 and B7-H4 are two novel members of the B7 superfamily that are actively involved in regulating the pathogenesis of infectious diseases. However, the intrahepatic expression of both members in HBV-ACLF patients has yet to be described. In this study, we analyzed the expression of B7-H3 and B7-H4 in HBV-ACLF biopsies by immunohistochemistry. Our results showed that both members were observed in all HBV-ACLF samples, and their expression was chiefly observed on infiltrating inflammatory cells and the damaged bile ducts. Immunofluorescence double staining showed that B7-H4 was expressed chiefly on CD3(+) T cells, CD68(+) macrophages, CK-18(+) bile ducts, and CD31(+) endothelial cells, while B7-H3 was found on all cell types detected. The expression of the programmed death (PD)-1 ligands, PD-L1 and PD-L2, was also detected in these liver tissues and they were found to be co-expressed with B7-H3 and B7-H4. These results suggest that the B7-family signaling is most likely to affect the pathogenesis of this disease, and a clear understanding of their functional roles may further elucidate the disease process.
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PMID:The characteristic expression of B7-H3 and B7-H4 in liver biopsies from patients with HBV-related acute-on-chronic liver failure. 2300 93

Although emperipolesis exists in infectious liver diseases, the diagnostic value of emperipolesis in chronic hepatitis B is not exactly known. The aim of this study is to evaluate the histological characteristics and laboratory parameters of emperipolesis in chronic hepatitis B. Totally 402 patients with hepatitis B and other liver diseases were processed in a retrospective assessment. Inflammatory severity of hepatitis B was evaluated with Ishak Scoring System. Immunofluorescent staining was performed for CD8 (T cells), CD20 (B cells), CD56 (NK cells), CD68 (macrophages) and MPO (neutrophils). Emperipolesis was observed in 74.0% of patients with chronic hepatitis B (CHB) and 82.8% of patients with acute hepatitis B (AHB). In emperipolesis, CD8(+) T cell was the main cell type. Patients with emperipolesis in CHB got high scores of inflammatory activity. Among patients with CHB, emperipolesis was present with higher serum ALT, AST and GGT levels. HBV DNA Load in patients with emperipolesis was as 10 times high as those without emperipolesis. HBeAb was significantly correlated with the evidence of emperipolesis. In chronic hepatitis B, emperipolesis was associated with severity of liver injury. The presence of emperipolesis was an indicator of active liver inflammation.
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PMID:Emperipolesis is a potential histological hallmark associated with chronic hepatitis B. 2651 3

The expression of cancer stemness is believed to reduce the efficacy of current therapies against hepatocellular carcinoma (HCC). Understanding of the stemness-regulating signaling pathways incurred by a specific etiology can facilitate the development of novel targets for individualized therapy against HCC. Niche environments, such as virus-induced inflammation, may play a crucial role. However, the mechanisms linking inflammation and stemness expression in HCC remain unclear. Here we demonstrated the distinct role of inflammatory mediators in expressions of stemness-related properties involving the pluripotent octamer-binding transcription factor 4 (OCT4) in cell migration and drug resistance of hepatitis B virus-related HCC (HBV-HCC). We observed positive immunorecognition for macrophage chemoattractant protein 1 (MCP-1)/CD68 and OCT4/NANOG in HBV-HCC tissues. The inflammation-conditioned medium (inflamed-CM) generated by lipopolysaccharide-stimulated U937 human leukemia cells significantly increased the mRNA and protein levels of OCT4/NANOG preferentially in HBV-active (HBV+HBsAg+) HCC cells. The inflamed-CM also increased the side population (SP) cell percentage, green fluorescent protein (GFP)-positive cell population, and luciferase activity of OCT4 promoter-GFP/luciferase in HBV-active HCC cells. Furthermore, the inflamed-CM upregulated the expressions of insulin-like growth factor-I (IGF-I)/IGF-I receptor (IGF-IR) and activated IGF-IR/Akt signaling in HBV-HCC. The IGF-IR phosphorylation inhibitor picropodophyllin (PPP) suppressed inflamed-CM-induced OCT4 and NANOG levels in HBV+HBsAg+ Hep3B cells. Forced expression of OCT4 significantly increased the secondary sphere formation and cell migration, and reduced susceptibility of HBV-HCC cells to cisplatin, bleomycin, and doxorubicin. Taking together, our results show that niche inflammatory mediators play critical roles in inducing the expression of stemness-related properties involving IGF-IR activation, and the upregulation of OCT4 contributes to cancer migration and drug resistance of HBV-HCC cells. Findings in this paper would provide potential targets for a therapeutic strategy targeting on inflammatory environment for HBV-HCC.
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PMID:Inflammation Promotes Expression of Stemness-Related Properties in HBV-Related Hepatocellular Carcinoma. 2812 44

Introduction It has been hypothesized that mental disorders including depression and anxiety can affect immune responses. The study was done to evaluate the relation between depression and anxiety and expression levels of CD36, CD68, and CD9 on peripheral blood monocytes of chronic hepatitis B (CHB) patients. Methods Sixty CHB patients were selected with various ranges of depression and anxiety. Depression and anxiety were evaluated using a standard questionnaire by an expert psychiatrist according to BECK's Depression Inventory II and Hamilton Anxiety Rating Scale, respectively. The levels of CD36, CD68, and CD9 on the peripheral blood monocytes have been performed using flow cytometry technique. Results The results demonstrated that levels of CD36 were significantly increased on the peripheral blood monocytes of CHB patients when compared with CHB patients with no anxiety. Expression levels of CD68 and CD9 were not significantly altered on the CHB patients with various ranges of anxiety. Expression levels of CD36, CD68, and CD9 were also not significantly altered on the CHB patients with various ranges of depression. Discussion It seems that anxiety induces inflammation in the CHB patients by induction of alteration in several molecules including up-regulation of CD36. CD36 plays important roles in the induction of tissue damage; hence, it may be hypothesized that anxiety may participate in the induction of some hepatitis B complications.
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PMID:Anxiety leads to up-regulation of CD36 on the monocytes of chronic hepatitis B-infected patients. 2862 84

Background/aim: This study aimed to investigate the potential regulatory role of prokineticin 2 (PK2) in modulation of the number and function of Kupffer cells (KCs) during the progression of liver fibrosis in patients with hepatitis B virus (HBV). Materials and methods: We obtained liver tissue sections from 200 patients with HBV undergoing surgical resection in our hospital between January 2013 and July 2016. Of these 200 tissue sections, 150 were fibrosis tissues and 50 were hepatocellular carcinoma tissues. Immunohistochemical evaluations were performed to assess the expression levels of CD68 and PK2 in the sections. The clinical parameters of these 200 patients were also analyzed. Results: As a potential cytokine, PK2 was commonly expressed in KCs. In addition, a close correlation between PK2 and the number of KCs during the progression of liver fibrosis in patients with HBV was found in this study. Conclusion: PK2 is expressed in KCs and participates in the progression of liver fibrosis after HBV infection. As a potential cytokine, PK2 modulates the number of KCs during fibrosis. Thus, PK2 most likely adjusts the number of M1 cells to modulate the role of KCs in the progression of liver fibrosis after HBV infection.
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PMID:Relationship between PK2 and number of Kupffer cells during the progression of liver fibrosis in patients with HBV 2947 55


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