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Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jul 7, 2008; 14(25): 4040-4046
Published online Jul 7, 2008. doi: 10.3748/wjg.14.4040
Composition of inflammatory infiltrate and its correlation with HBV/HCV antigen expression
Bozena Walewska-Zielecka, Kazimierz Madalinski, Joanna Jablonska, Paulina Godzik, Joanna Cielecka-Kuszyk, Bogumila Litwinska
Bozena Walewska-Zielecka, Kazimierz Madalinski, Paulina Godzik, Joanna Cielecka-Kuszyk, Bogumila Litwinska, Department of Virology, National Institute of Public Health, National Institute of Hygiene, Warsaw 00-791, Poland
Joanna Jablonska, Department of Hepatology and AIDS, Warsaw Medical University, Warsaw 01-201, Poland
Author contributions: Walewska-Zielecka B designed and performed research; Madalinski K and Godzik P equally contributed to write the paper; Jablonska J collected the patient data; Cielecka-Kuszyk J contributed to data interpretation and wrote parts of the paper; Litwinska B contributed to data interpretation and collection of funds.
Correspondence to: Kazimierz Madalinski, Laboratory of Viral Immunopathology, Department of Virology, National Institute of Public Health, National Institute of Hygiene, Warsaw 00-791, Poland. kmadalinski@pzh.gov.pl
Telephone: +48-22-5421326
Fax: +48-22-5421237
Received: February 27, 2008
Revised: June 17, 2008
Accepted: June 24, 2008
Published online: July 7, 2008
Abstract

AIM: To study the composition of liver inflammatory infiltrate in biopsy material from patients chronically infected with hepatotropic viruses and to evaluate the correlation of inflammatory infiltrate with hepatitis B virus (HBV) and hepatitis C virus (HCV) viral antigen expression in chronic B and C hepatitis.

METHODS: The phenotype of inflammatory cells was evaluated by the EnVision system, using a panel of monoclonal antibodies. HBV and HCV antigens were detected with the use of monoclonal anti-HBs, polyclonal anti-HBc and anti-HCV antibodies, respectively.

RESULTS: The cellular composition of liver inflammatory infiltrate was similar in the patients with B and C hepatitis: ~50%-60% of cells were T helper lymphocytes. Approximately 25% were T cytotoxic lymphocytes; B lymphocytes comprised 15% of inflammatory infiltrate; other cells, including NK, totalled 10%. Expression of HLA antigens paralleled inflammatory activity. Portal lymphadenoplasia was found more often in hepatitis C (54.5%) than in hepatitis B (30.6%). Expression of HBcAg was found more often in chronic B hepatitis of moderate or severe activity. Overall inflammatory activity in HBV-infected cases did not correlate with the intensity of HBsAg expression in hepatocytes. Inflammatory infiltrates accompanied the focal expression of HCV antigens. A direct correlation between antigen expression and inflammatory reaction in situ was noted more often in hepatitis C than B.

CONCLUSION: Irrespective of the etiology and activity of hepatitis, components of the inflammatory infiltrate in liver were similar. Overall inflammatory activity did not correlate with the expression of HBsAg and HCVAg; HBcAg expression, however, accompanied chronic hepatitis B of moderate and severe activity.

Keywords: Chronic B and C hepatitis; Inflammatory infiltrate; Lymphoid follicle; Lymphadenoplasia