Influx of macrophages into livers of rats treated with hepatotoxicants (thioacetamide, allyl alcohol, D-galactosamine) induces expression of HSP25.

Treatment of rats with a single dose of thioacetamide (TAA) provokes centrilobular inflammation and a significant expression of heat shock protein HSP25 in hepatocytes surrounding the area of inflammation. The HSP25 accumulation in hepatocytes adjacent to inflammatory regions was confirmed by identification of positive hepatocytes concentrated at periportal areas after treatment of rats with allyl alcohol (AA) or distributed diffusely throughout liver lobule after treatment with D-galactosamine (D-gal). In our model of TAA-treated rats the use of the anti-inflammatory drug-indomethacin, and the redox-regulating drug-N-acetylcysteine (NAC), significantly attenuated TAA-induced HSP25 expression and evoked morphological changes of recruited ED1+ macrophages. Treatment of rats with gadolinium chloride (GdCl(3)) decreased considerably the number of Kupffer cells (ED2+ macrophages) without affecting significantly the number and morphology of ED1+ macrophages as well as the expression pattern of TAA-induced HSP25. Our data shows for the first time that ED1+ macrophages recruited into the liver by treatment with TAA play a significant role in HSP25 induction in hepatocytes.