Role of caspase-8 in hepatocyte response to infection and injury in mice

Tehila Ben Moshe, Hila Barash, Tae Bong Kang, Jin Chul Kim, Andrew Kovalenko, Eitan Gross, Marcus Schuchmann, Rinat Abramovitch, Eithan Galun, David Wallach*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

71 Scopus citations


Caspase-8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase-8 gene specifically in the liver, we found that caspase-8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes, attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the proliferation of hepatocytes, although initially suppressed, might later be persistently enhanced, resulting in significant hepatomegaly. Conclusion: These findings indicate that caspase-8 participates in regulation of the cellular response to infection and injury and that it does so by affecting various cellular functions, including cell death, cell proliferation, and induction of inflammation.

Original languageAmerican English
Pages (from-to)1014-1024
Number of pages11
Issue number4
StatePublished - Apr 2007
Externally publishedYes


Dive into the research topics of 'Role of caspase-8 in hepatocyte response to infection and injury in mice'. Together they form a unique fingerprint.

Cite this