Kupffer cells from CC1(4)-treated XXXX livers induce skin fibroblast and liver fat-storing cell proliferation in culture.

@entity82 @entity4059 @entity665 @entity3812 @entity35 @entity3352
Conditioned media of Kupffer cells from normal @entity35 liver produce in culture two factors that inhibit fibroblast proliferation. The inhibitory factors have molecular masses of approximately 25 and 5 kDa. In contrasts to these results, the conditioned media of Kupffer and mononuclear macrophagic cells, obtained 48 hours after CC1(4) administration to @entity35 , contains a 17 kDa @entity4059 ( @entity4059 ). @entity4059 also stimulates @entity665 incorporation into DNA of cultured @entity35 liver fat-storing cells. Two peaks with @entity4059 activity were demonstrated after isoelectrofocusing; one with a pI of 6.1 and a second with a pI of 7.5. The fraction containing @entity4059 is devoid of interleukin-1 (IL-1) activity and no inhibitory activity is detected in this conditioned media. Production of @entity4059 is inhibitable by @entity3812 but not by @entity3352 , it is thermolabile and trypsin-sensitive. In animals treated chronically with CC1(4) to produce @entity82 , @entity4059 activity is demonstrable from the first to the 8th week of treatment. However, the activity is lower at 8 weeks post-CC1(4) as compared with 2 weeks. The results suggest that homeostasis of cells in the liver is controlled by factors produced locally, that act by autocrine and paracrine mechanisms. When homeostasis is altered, fibroblast proliferation occurs, and excess collagen deposition leads to @entity82 . We propose that the antifibrogenic activity of @entity3812 is associated, in part, with its capacity to inhibit the release of @entity4059 by Kupffer cells and liver mononuclear macrophage cells.
