HepG2 hepatocytes express IFN-γ, TNF-α, TGF-β, M-CSF, oncostatin-M, ICAM-1, IL-4, IL-5, IL-7, IL-10, IL-11, IL-12 and IL-6 receptor genes in vitro

S Russwurm¹, I Stonans¹, E Stonane², G Weigand¹, M Wiederhold¹, L Jäger² and K Reinhart ¹

¹Department of Anesthesiology and Intensive Therapy, Friedrich-Schiller-University of Jena, 07740 Jena, Germany

²Institute of Clinical Immunology, Friedrich-Schiller-University of Jena, 07740 Jena, Germany

from 18th International Symposium on Intensive Care and Emergency Medicine
Brussels, Belgium. 17–20 March 1998

Critical Care 1998, 2(Suppl 1):P005doi:10.1186/cc135

Published:

1 March 1998

Introduction

Pro- and antiinflammatory cytokines are known to be involved in the pathogenesis of septic shock and multiple organ dysfunction, including liver failure. Many lympho- and monokines may alter hepatocellular function. Liver parenchymal cells themselves, in contrast to mononuclears like Kupffer cells, are generally considered only targets but not producers of these important mediators.

Methods

In order to investigate whether hepatocellular cells are a potential source of various regulatory cytokines we have estimated the multiple cytokine gene expression in the culture of well differentiated human HepG2 hepatoma cells using RT-PCR.

Results

Our findings demonstrate that HepG2 cells express mRNAs for IFN-γ, TNF-α, TGF-β, M-CSF, oncostatin-M, ICAM-1, IL-4, IL-5, IL-7, IL-10, IL-11, IL-12 and IL-6R. At the same time the expression of IL-1, IL-2, IL-3, IL-6, CD40 ligand and IL-2R genes was not detected.

Conclusions

Hepatocytes are potential producers of a variety of cytokines, some of them being able to regulate hepatocellular functions directly, others are important regulators of leukocyte functions. Thus, on the one hand, hepatocytes may express autoregulatory cytokines and, on the other hand, influence the functions of other liver cells like Kupffer, Ito or endothelial cells. Due to their large amount, liver parenchymal cells could be an important source of systemically acting pro- and anti-inflammatory and other regulatory cytokines.

Acknowledgement

Supported in part by grants from the Deutsche Forschungsgemeinschaft (Re 653/5-1) and the Thuringian Ministry of Science, Research and Culture (B301-95026).