Lipid accumulation in concanavalin A-induced hepatitis: Another cause for impaired liver regeneration afterwards?

Authors

  • Dechun Feng,

    1. Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiaotong University School of Medicine, Shanghai, China
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  • Lingyun Xu

    1. Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiaotong University School of Medicine, Shanghai, China
    2. Shanghai Institute of Immunology, Shanghai Jiaotong University School of Medicine, Shanghai, China
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  • Potential conflict of interest: Nothing to report.

Lipid Accumulation in Concanavalin A-Induced Hepatitis: Another Cause for Impaired Liver Regeneration Afterwards?

To the Editor:

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).

Figure 1.

Increased lipid accumulation in CIH mice. ConA (15 mg/kg body weight) was injected intravenously into C57BL/6 mice. Four days later, frozen liver sections (8 μm) were obtained from naïve and ConA-treated mice. (A) Oil Red O staining of liver sections (400×). Arrows indicate lipid droplets stained by oil Red O. (B) Image analysis of lipid accumulation. The extent of labeling in the liver lobule was defined as the percent of the field area within the default color range. Data from each tissue section (5 fields per section) were pooled to determine means (**P < 0.01).

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.

Dechun Feng*, Lingyun Xu* †, * Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiaotong University School of Medicine, Shanghai, China, † Shanghai Institute of Immunology, Shanghai Jiaotong University School of Medicine, Shanghai, China.

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