Washington: A new study has found that dendritic cells in the liver have a protective role against the toxicity of acetaminophen, the widely used over-the-counter pain reliever and fever reducer for adults and children.
High-doses of acetaminophen can cause hepatotoxicity, chemical driven liver damage.
NYU School of Medicine researchers found an abundance of dendritic cells in the liver can protect the organ from acetaminophen damage while low levels of dendritic cells in the liver are associated with exacerbated liver damage, liver cell and tissue death, known as centrilobular hepatic necrosis, and acute liver failure from acetaminophen.
“Our research results confirm a central role for dendritic cells and their powerful regulation of acetaminophen’s toxicity,” said George Miller, MD, senior author of study and assistant professor, Departments of Surgery and Cell Biology at NYU Langone Medical Center.
“High levels of dendritic cells have a novel, critical and innate protective role in acetaminophen hepatotoxicity. We now have greater insight into the liver’s tolerance of acetaminophen toxicity and dendritic cell regulation of these toxins,” he stated.
Researchers discovered dendritic cell depletion exacerbates acetaminophen``s damage to the liver.
The acetaminophen treated mice with depleted dendritic cells had more extensive liver cell and tissue death compared to other mice.
Also, these mice died within 48 hours of acetaminophen challenge whereas death was rare in other mice without dendritic cell depletion.
In addition, the study shows dendritic cell expansion successfully diminished the hepatotoxic effects of acetaminophen protecting the liver from damage.
The findings have been published in the September issue of the journal Hepatology.