Association of NK Cells with the Severity of Fibrosis in Patients with Chronic Hepatitis C.

Some NK cell subpopulations may be involved in the modulation of fibrogenesis in the liver. The aim of the study was to evaluate the relationship between the number and phenotype of NK cell subsets in peripheral blood (PB) and total NK cell percentage, population density and the degree of liver fibrosis of patients infected with hepatitis C virus (HCV+). The study group consisted of 56 HCV+ patients, divided into two subgroups: patients with mild or moderate fibrosis and patients with advanced liver fibrosis or cirrhosis (F ≥ 3 in METAVIR classification). The preparations were stained with H-E and AZAN staining. NK cells were targeted with anti-CD56 antibody and identified automatically in situ using the DakoVision system. Assessment of different NK cell subsets in PB was performed with the flow cytometry technique. In the PB of HCV+ patients with advanced liver fibrosis, there was a lower proportion of CD62L+; CD62L+/CD94++; CD27+; CD127+/CD27+ and CXCR3+/CD27+ NK subsets, as compared to patients with mild/moderate liver fibrosis. The results also showed no association between total PB NK cell level and total intrahepatic NK cell population density between patients with mild/moderate fibrosis and with advanced liver fibrosis. However, positive correlations between the PB levels of CD94+ and CD62L+ NK cell subsets and the intrahepatic total NK cell percentage and population density in the liver, irrespectively to the extent of fibrosis, were observed. Additionally, positive correlation was found between the PB CXCR3+/CD94+ NK cell percentages and intrahepatic NK cell percentages in patients with advanced hepatic fibrosis. Lower blood availability of specific NK subsets in patients with chronic type C hepatitis might be a cause of progression of liver fibrosis via insufficient control over hepatic stellate cells.

Multiple gingival recession coverage with an allogeneic biostatic fascia lata graft using the tunnel technique--A histological assessment.

BACKGROUND: Autogenous connective tissue graft (CTG) that can be safely harvested from the palatal mucosa is limited. Often a multi-stage surgical procedure is needed to cover multiple gingival recessions (MGR). To address this problem, efforts are being made to explore substitutes suitable in size to ensure surgical treatment in a single visit.The objective of the present study was the histological evaluation of tissue in the recipient site after augmentation with a hydrated biostatic Fascia Lata Allograft (FLA) in conjunction with MGR coverage at different healing stages. MATERIAL AND METHODS: Twelve patients needing bilateral multiple gingival recession coverage participated in this study. On the test side, the tunnel technique with FLA was used, while CTG, harvested from the palatal mucosa, was used to cover MGR on the control side. Histological assessment was performed 3, 6, 9 and 12 months after augmentation. RESULTS: FLA was well tolerated by the host tissue. During all investigation periods histological images of all patients in the test side revealed a slow process of incorporation of the material grafted in the host connective tissue, showing a colonization of the graft with host fibroblasts and formation of new blood vessels. After 12 months, the graft had fully remodeled into connective tissue of the host gingiva. CONCLUSION: Apart from the limitations of the present study, we conclude that the FLA may serve as a substitute for autogenous CTG harvested from the palatal mucosa and can be applied as a technique for covering MGR in a single visit.

Association between hepatic angiogenesis and serum adipokine profile in non-obese chronic hepatitis C patients.

It is unclear whether angiogenesis merely represents a homeostatic mechanism aimed at ensuring an adequate oxygen supply or one that exerts an additional pathogenic role leading to liver damage in chronic hepatitis. Chronic hepatitis C (CHC) patients present a proangiogenic profile of angiogenic markers. Adipokines not only regulate adipose tissue and glucose metabolism, but also influence inflammation, fibrogenic process and production of proangiogenic factors. On the basis of this evidence we aimed to assess the number of new blood vessels in lobules and portal tracts in the liver and evaluate the relationship between angiogenesis intensity and serum adipokine concentrations in CHC. Our study showed a positive association between serum vaspin and angiogenesis intensity in portal tracts and lobules in CHC patients (r = 0.41, p = 0.04; r = 0.46, p = 0.03; respectively). Serum visfatin was found to be negatively related to angiogenesis in portal tracts and lobules but only in females (r = -0.76, p = 0.03; r= -0.95, p < 0.001; respectively). In conclusion, the role of some adipokines in liver angiogenesis seems to be different in females than in males. Serum vaspin concentration seems to reflect intensity of liver angiogenesis in CHC. Further studies are necessary to better determine the role of adipokines in new blood vessel formation in CHC.

Hepatocyte steatosis in HCV patients promotes fibrosis by enhancing TGF-beta liver expression.

AIM: The objective of this study was to examine the relationship between TGF-beta expression in steatotic liver and the stage and yearly progression rate of fibrosis in chronic hepatitis C (CHC) patients. METHODS: We examined 44 CHC fatty liver patients, using 76 non-steatotic CHC patients as controls. The stage of hepatic fibrosis was assessed on a score scale. TGF-beta expression was determined with the use of monoclonal serum and the ABC three-step method. RESULTS: We demonstrated a positive correlation of steatosis with the stage of fibrosis (P < 0.05). No relationship of thiskind was found with the yearly progression rate of fibrosis (P > 0.09). In steatotic biopsies, TGF-beta expression index in portal spaces and lobules was found to be higher as compared to TGF-beta expression in biopsies without steatosis (P < 0.05). CONCLUSION: In CHC patients steatosis induces the development of fibrosis by elevating the hepatic expression of TGF-beta.