Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Gastroenterology. 2002 Jun;122(7):2001-10.

Critical role of interleukin 5 and eosinophils in concanavalin A-induced hepatitis in mice.

Author information

  • 1Laboratory of Experimental Gastroenterology, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium. hlouis@ulb.ac.be

Abstract

BACKGROUND & AIMS:

Eosinophils are observed in several liver diseases, but their contribution in the pathogenesis of these disorders remains poorly investigated. Concanavalin A (Con A)-induced hepatitis is an experimental model of immune-mediated liver injury in which natural killer T (NKT) cells play a critical role through the production of interleukin (IL)-4 and the expression of Fas ligand (FasL). Because activated NKT cells also produce IL-5, a critical cytokine for eosinophil maturation and function, the role of IL-5 was investigated in this model.

METHODS:

IL-5-deficient mice, eosinophil depletion in wild-type (WT) mice, and NKT cell transfer from WT- or IL-5-deficient mice into NKT cell-deficient mice were used to assess the role of IL-5 and eosinophils.

RESULTS:

Liver eosinophil infiltrate and IL-5 production were observed after Con A challenge. Liver injury was dramatically reduced in IL-5-deficient or eosinophil-depleted mice. In addition, residual hepatitis observed in Fas-deficient mice was abolished after IL-5 neutralization. Finally, we showed that NKT cells constituted a critical source of IL-5. Indeed, transfer of WT NKT cells to mice lacking NKT cells restored liver injury, whereas transfer of IL-5-deficient NKT cells did not.

CONCLUSIONS:

These observations highlight the pathologic role of IL-5 and eosinophils in experimental immune-mediated hepatitis.

PMID:
12055605
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk