IL-1β and TNF-α produced by peripheral blood mononuclear cells before and during interferon therapy in patients with chronic hepatitis C
We investigated the spontaneous and phytohemagglutinin-stimulated production of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) by peripheral blood mononuclear cells in patients with chronic hepatitis C during treatment with interferon-α (IFN-α). Spontaneous productions of these were significantly higher in patients with chronic hepatitis C than in healthy subjects. For patients prescribed interferon, stimulated production of TNF-α was significantly higher in complete responders than in partial responders, but the differences were small between the other cytokine levels and outcome of IFN treatment. Spontaneous production of these cytokines was higher in patients with genotype III with complete response than in genotype III patients with a partial response, but this was not the case in patients with genotype II. There was a negative correlation between these cytokines and histological activity index. Spontaneous production of cytokines was decreased only in complete responders after the administration of interferon. These data suggest that the elevated production of cytokines in patients with chronic hepatitis C may be due to host response to the virus, and monitoring cytokines along with alanine aminotransferase and hepatitis C virus RNA during treatment may provide more precise information of the effectiveness of therapy.
Key wordschronic hepatitis C interferon therapy IL-1 TNF
Unable to display preview. Download preview PDF.
- 8.Lazzari FD, Fabris P, Floreani A, Bortolami M, Venturi C, Chiaramonte M, Naccarato R: Tumor necrosis factor-alpha behavior in serum during recombinant-alpha-2b-interferon treatment of chronic viral hepatitis. Eur J Gastroenterol Hepatol 6:625–628, 1994Google Scholar
- 9.Daniels HM, Meager A, Eddelston ALWF, Alexander GJM, Williams R: Spontaneous production of tumor necrosis factor alpha and interleukin-1 beta during interferon-alpha treatment of chronic HBV infection. Lancer 335:875–877, 1990Google Scholar
- 11.Oppenheim JJ, Kovaks EJ, Matsushima K, Durum SK: There is more than one interleukin 1. Immunol Today 7:45–56, 1986Google Scholar
- 16.Hayashi J, Nakashima K, Noguichi A, Hirata M, Akazawa K, Kashiwagi S: Antiviral effect of interferon therapy for patients with chronic hepatitis C. Antiviral Chem Chemother 3:305–309, 1992Google Scholar
- 19.Okamoto H, Sugiyama Y, Okada S, Kurai K, Akahane Y, Sugai Y, Tanaka T, Satoh K, Tsuda F, Miyakawa Y, Mayumi M: Typing hepatitis C virus by polymerase chain reaction with type-specific primers: Application to clinical surveys and tracing infectious sources. J Gen Virol 73:673–679, 1992PubMedGoogle Scholar
- 21.Tanaka K, Ishikawa E, Ohmoto Y, Hirai Y:In vitro production of human interleukin 1α and interleukin 1β by peripheral blood mononuclear cells examined by sensitive sandwitch enzyme immunoassay. Eur J Immunol 17:1527–1530, 1989Google Scholar
- 22.Takehara T, Hayashi N, Mita E, Hagiwara H, Ueda K, Katayama K, Kasahara A, Fusamoto H, Kamada T: Detection of the minus strand of hepatitis C virus RNA by reverse transcription and polymerase chain reaction: Implications for hepatitis C virus replication in infected tissue. Hepatology 15:387–390, 1992PubMedGoogle Scholar