Year 2006 / Volume 98 / Number 6
Puntos De Vista
Kupffer cells and alcoholic liver disease

pp. 460-472

F. J. Cubero and N. Nieto

Abstract
Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development
of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut’ increasing plasma and liver endotoxin
levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling
to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase
metabolites, and reactive oxygen species such as
superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects
on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as
upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and
reparative responses. Thus, the homeostatic responses are initiated
by Kupffer cell-derived mediators at the cellular level and underlie the liver’s defense and reparative mechanisms against injury.
In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated,
and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic
liver disease.
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