Kupffer cell inactivation ameliorates immune liver injury via TNF- α/TNFR1 signal pathway in trichloroethylene sensitized mice.

Kupffer cell inactivation ameliorates immune liver injury via TNF-α/TNFR1 signal pathway in trichloroethylene sensitized mice. Immunopharmacol Immunotoxicol. 2020 Aug 18;:1-27 Authors: Zhang JX, Xu QY, Yang Y, Li N, Zhang Y, Deng LH, Zhu QX, Shen T Abstract In our previous studies, we found that Kupffer cell activation and tumor necrosis factor (TNF)-α was increased in liver which took an important role in immune liver injury in Trichloroethylene (TCE) sensitized mice. However, the exact effect of them was not revealed yet. Thus, we select a Kupffer cell activity inhibitory drug, gadolinium chloride (GdCl3), to explore the important role of Kupffer cell and its related cytokine TNF-α. We found F4/80, the marker of Kupffer cell, was increased in TCE positive group. GdCl3 treatment successfully blocked the activation of Kupffer cell. TNF-α was increased significantly in liver of TCE sensitized mice and decreased significantly when low-dose GdCl3 was used. We found TNF receptor 1 (TNFR1) was increased significantly and GdCl3 treatment resumed the expression of TNFR1 to normal level, as well as the F4/80, TNF-α and TNFR1 mRNA. We also found both caspase-8 and caspase-3 increased in TCE positive group and decreased in TCE + GdCl3 positive group. The number of apoptotic cells in TCE sensitized mice increased by TUNEL staining, and GdCl3 treatment alleviated this increase. Some cells showed edema and inflammatory cell aggregation i...
Source: Immunopharmacology and Immunotoxicology - Category: Allergy & Immunology Tags: Immunopharmacol Immunotoxicol Source Type: research