Published online Nov 15, 2015. doi: 10.4291/wjgp.v6.i4.90
Peer-review started: May 27, 2015
First decision: July 3, 2015
Revised: July 27, 2015
Accepted: September 7, 2015
Article in press: September 8, 2015
Published online: November 15, 2015
Kupffer cells play a central role in the pathogenesis of alcoholic hepatitis (AH). It is believed that alcohol increases the gut permeability that results in raised levels of serum endotoxins containing lipopolysaccharides (LPS). LPS binds to LPS-binding proteins and presents it to a membrane glycoprotein called CD14, which then activates Kupffer cells via a receptor called toll-like receptor 4. This endotoxin mediated activation of Kupffer cells plays an important role in the inflammatory process resulting in alcoholic hepatitis. There is no effective treatment for AH, although notable progress has been made over the last decade in understanding the underlying mechanism of alcoholic hepatitis. We specifically review the current research on the role of Kupffer cells in the pathogenesis of AH and the treatment strategies. We suggest that the imbalance between the pro-inflammatory and the anti-inflammatory process as well as the increased production of reactive oxygen species eventually lead to hepatocyte injury, the final event of alcoholic hepatitis.
Core tip: In this editorial we provide critical comments on the pivotal role of Kupffer cells on the development of alcoholic hepatitis with a focus on the pro-inflammatory as well as the anti-inflammatory pathways. We propose that the anti-inflammatory pathway should be further explored as a potential alternative for novel treatment strategies. This editorial is significant as it provides a platform for the future basic and clinical research in elucidating the pathogenesis and developing the management strategies of this common clinical pathology - alcoholic hepatitis.