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Altered Expression of SHIP, a Toll-like Receptor Pathway Inhibitor, Is Associated With the Severity of Liver Fibrosis in Chronic Hepatitis C Virus Infection

  1. Author:
    Katsounas, A.
    Trippler, M.
    Kottilil, S.
    Lempicki, R. A.
    Gerken, G.
    Schlaak, J. F.

  2. Author Address

    [Katsounas, A; Trippler, M; Gerken, G; Schlaak, JF] Univ Hosp Essen, Dept Gastroenterol & Hepatol, D-45147 Essen, Germany. [Katsounas, A; Lempicki, RA] NCI Frederick, SAIC Frederick Inc, Lab Immunopathogenesis & Bioinformat, Frederick, MD USA. [Kottilil, S] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.;Schlaak, JF (reprint author), Univ Hosp Essen, Dept Gastroenterol & Hepatol, Hufelandstr 55, D-45122 Essen, Germany;joerg.schlaak@uni-due.de
    1. Year: 2011
    2. Date: Oct
  2. Journal: Journal of Infectious Diseases
    1. 204
    2. 8
    3. Pages: 1181-1185
  4. Type of Article: Article
  5. ISSN: 0022-1899
  1. Abstract:

    Hepatitis C-related fibrogenesis has been shown to involve complex interactions between peripheral and hepatic immune responses. Peripheral whole blood (PB) samples from patients with chronic hepatitis C (n = 36) were subjected to microarray analysis in order to identify gene expression patterns associated with immune pathways in PB and hepatic fibrosis. Distinct regulation of gene expression of inositol polyphosphate-5-phosphatase/145kDa (INPP5D or SHIP), a TLR2/TLR4-inhibitor, and heat shock protein 8/22kDa (HSPB8), an endogenous TLR4-ligand, during fibrogenesis was identified and could be confirmed by quantitative reverse-transcription polymerase chain reaction. These results suggest a potential link between peripheral activity of the TLR4-pathway, peripheral SHIP-dependent immune regulation, and liver fibrosis.

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External Sources

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  2. DOI: 10.1093/infdis/jir500
  3. View record in Web of Science®
  4. WOS: 000294970100006

Library Notes

  1. Fiscal Year: FY2011-2012
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