We read with interest the article by Hines et al. on impaired liver regeneration in T cell–mediated hepatitis.1 The authors observed an interesting phenomenon that mice injected with concanavalin A (ConA) showed impaired liver regeneration 4 days after injection. They also found that important factors in liver regeneration such as cyclin D, pStat3, and interleukin-6 were reduced in ConA-induced hepatitis (CIH), whereas inhibitors of hepatocyte proliferation such as p21, Smad2, tumor growth factor β and interferon γ were increased. The authors attributed the mechanisms to the modulation of oval cells by ConA treatment.
We set up a CIH model in C57BL/6 mice following the authors' protocol. Four days after ConA injection, we obtained liver sections from both naïve and ConA-treated mice, and then performed oil Red O staining for lipid deposits. Much more accumulated lipid was seen in CIH mice (Fig. 1).
DeAngelis et al.2 have reported that liver regeneration was impaired in mice with fatty liver. This finding was supported by several recent studies.3–5 Although detailed mechanisms need further investigation, the relationship between fatty liver and impaired liver regeneration was well established. Therefore, it will be interesting to investigate whether lipid accumulation also contributes to impaired liver regeneration in CIH mice.
It is well known that hepatic steatosis was associated with hepatitis B and hepatitis C virus infections.6 Studies on the interactions between liver infection, lipid accumulation, and liver regeneration will surely improve our knowledge about liver injury and repair, and bring great benefits to the treatment and prevention of liver diseases.