[KCTD9, a novel potassium channel related gene, was highly expressed in hepatic NK cells and T cells of fulminant hepatitis mice induced by MHV-3].

OBJECTIVE: To explore the mechanisms of a novel potassium channel gene named KCTD9 (potassium channel tetramerization domain containing 9) in model of fulminant viral hepatitis induced by murine hepatitis virus 3 (MHV-3). METHODS: 78 BALB/cJ mice(6 male) were randomly and equally assigned to two groups, model group of fulminant viral hepatitis induced by MHV3 and its control. 75 C3H/HeJ female mice were done into two groups, 39 for model group of chronic hepatitis induced by MHV3, 36 for control. Various samples including spleen, liver and lymphocytes from mice of two model groups and the controls were examined for KCTD9 expression by real time quantitative PCR and Immunohistochemistry. Independent-samples T test or one-way ANOVA were carried out in different groups. RESULTS: Increased expressions of KCTD9 mRNA was observed in livers of both model mice of fulminant viral hepatitis and chronic hepatitis. Compared with the control mice, the expressions of KCTD9 mRNA were up-regulated by 577.1-, 8.8-, 59.4- and 10.8-fold in hepatic NK cells, CD4+ T cells, CD8+ T cells and splenic NK cells respectively in model mice of fulminant viral hepatitis 48 hr post MHV-3 infection, whereas down-regulation by 43% and 69% in splenic CD4 + T cells and CD8+ T cells were found respectively. In contrast, in model mice of chronic viral hepatitis the expressions of KCTD9 mRNA were down-regulated by 71% and 51% in hepatic CD4+ T cells and NK cells, respectively. The expression of KCTD9 protein was mainly evidenced in infiltrative mononuclear cells of liver as shown by immunohistochemistry. Basal expression was also investigated and showed constitutive expression of KCTD9 in brain, thymus and other organs in BALB/cJ mice. CONCLUSION: A novel potassium channel gene KCTD9 was highly expressed in hepatic NK cells and T cells of fulminant hepatitis mice induced by MHV-3.

[Increased expression of KCTD9, a novel potassium channel related gene, correlates with disease severity in patients with viral hepatitis B].

OBJECTIVE: Studies have shown that potassium channel plays a pivotal role in T cell activation. The expression of potassium channel gene KCTD9 was evidenced being highly upregulated in patients with severe hepatitis B (SHB). To understand this phenomenon further, tissue and cellular expression profiles of KCTD9 were investigated in patients with SHB. METHODS: A rabbit peptide polyclonal antibody was prepared. Various samples including peripheral blood mononuclear cells (PBMCs); livers from patients with SHB or mild chronic hepatitis B, were examined for KCTD9 expression by quantitative real time PCR and immunohistochemistry staining (IHC). Confocal microscopy was used to illustrate the localizations of the expressions. RESULTS: Increased expression of KCTD9 was observed in PBMC in over 35.7% of the patients with SHB when compared with that of patients with mild chronic hepatitis B. In all patients, the relative value of increased KCTD9 mRNA was positively correlated with alanine aminotransferase, aspartate aminotransferase, total bilirubin and direct bilirubin but negatively with serum albumin. The expression was mainly located in hepatocytes, bile duct epithelial cells, Kupffer cells and inflammatory cells, and in the cytoplasm of PBMCs from the healthy individuals and patients with mild chronic hepatitis B, whereas in both cytoplasm and nuclei in those from patients with SHB. CONCLUSION: The increased expression of potassium channel gene KCTD9 correlates with disease severity in patients with viral hepatitis B.

[Relationship between hepatitis B virus in gastric mucosa and syndrome of disharmony between liver and stomach in patients with chronic hepatitis B].

OBJECTIVE: To study the relationship between the infection of hepatitis B virus (HBV) in gastric mucosa and the syndrome of disharmony between liver and stomach. METHODS: Subjects were divided into 2 groups: 30 patients with chronic hepatitis B (CHB) and the syndrome of disharmony between liver and stomach in hepatitis group, and 30 patients with chronic gastritis and the syndrome of disharmony between liver and stomach in gastritis group. Liver function and the markers of HBV were detected. The contents of HBV-DNA in serum and in gastric mucosa were assayed respectively by fluorescence quantitative polymerase chain reaction (FQ-PCR). RESULTS: (1) The incidence of gastric mucosal lesion in hepatitis group was up to 96.7% (29/30). (2) Scores of the syndrome of disharmony between liver and stomach in hepatitis group were significantly lower than those in gastritis group (P<0.05). The positive rates of HBV-DNA in serum, gastric fundus, body and antrum were 56.7%, 76.7%, 76.7% and 70.0%, respectively. (3) A positive correlation was found not only among the content of HBV-DNA in serum and the contents of HBV-DNA in gastric mucosa (r=0.66-0.94, P<0.01), but also among the contents of HBV-DNA in serum, gastric mucosa and the total score of the syndrome of disharmony between liver and stomach in hepatitis group (r=0.36-0.52, P<0.05). CONCLUSION: The infection of HBV is involved in the syndrome of disharmony between liver and stomach. Gastric mucosal lesion is universal in CHB patients with the syndrome of disharmony between liver and stomach.