Hepatic stellate cell activation and liver fibrosis are associated with necroinflammatory injury and Thl‐like response in chronic hepatitis C

Wiley - Tập 19 Số 3 - Trang 212-219 - 1999
Gianluca Svegliati‐Baroni1, Alfredo Pastorelli1, Aldo Manzin2, A. Benedetti1, Luca Marucci1, Laura Solforosi2, A. Di Sario1, E. Brunelli1, F. Orlandi1, Massimo Clementi3, Giampiero Macarri1
1Department of Gastroenterology, University of Trieste, Italy
2Institute of Microbiology, University of Ancona, Italy
3Department of Biomedical Sciences, University of Trieste, Italy

Tóm tắt

Abstract: Background/Aims: The involvement of a direct viral cytopathic effect or an immune‐mediated mechanism in the progression of hepatic damage in chronic hepatitis C is controversial. The type of immune response is itself a matter of controversy, and histological data are lacking. The aim of this study was to identify the factors associated with the progression of liver injury in 30 HCV/RNA‐positive untreated patients with chronic hepatitis. Methods: Necroinflammatory and architectural damage were evaluated using Ishak's score. Activated hepatic stellate cells (HSC) were visualized by immunohistochemistry for α‐smooth muscle actin (αSMA) and quantitated by morphometry. Plasma HCV/RNA was evaluated using a competitive RT‐PCR method. To study the type of immune response involved in the progression of liver injury, interferony (IFNγ)‐positive cells (as expression of a Th1‐like response) were evaluated by immunohistochemistry and quantitated by morphometry. Results: HSC were mostly detected close to areas of lobular necroinflammation or lining fibrotic septa. The αSMA‐ and Sirius Red‐positive parenchyma correlated significantly with necroinflammatory and architectural scores. IFNγ‐positive cells were detected in periportal areas associated with the inflammatory infiltrates and significantly correlated with architectural damage. No relationship was found between the histological features of liver injury and viral load. Conclusions: HSC activation and progression of liver injury are unrelated to viral load but associated with a Th1‐like response, a plausible target for the treatment of chronic hepatitis C.

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