ABSTRACT
Injury to the liver is a multifaceted process involving complex interactions among several different cell types and endogenous mediators. Cells involved in liver injury include liver cells: hepatocytes, Kupffer cells, and endothelial cells, as well as circulating leukocytes such as monocytes and neutrophils. Liver injury begins with a chemical, bacterial, or pathophysiological insult which initiates damage to liver cells, particularly hepatocytes. Initial damage to hepatocytes leads to re lease of cytoplasmic mediators resulting in Kupffer cell activation and leukocyte recruitment. Activated Kupffer cells and infiltrating leukocytes respond by re leasing even more endogenous mediators, including reactive oxygen and nitro gen radicals (1,2,) proteases (3), leukotrienes (4), prostaglandins (5), and cytokines (6,7). Release of these mediators ultimately results in potentiation of the initial liver damage. In particular, cytokines released by activated Kupffer cells and recruited leukocytes play a pivotal role in exacerbation of a nontoxic insult to the liver.
