Impact of NKT Cells and LFA-1 on Liver Regeneration under Subseptic Conditions

PLoS One. 2016 Dec 15;11(12):e0168001. doi: 10.1371/journal.pone.0168001. eCollection 2016.

Abstract

Background: Activation of the immune system in terms of subseptic conditions during liver regeneration is of paramount clinical importance. However, little is known about molecular mechanisms and their mediators that control hepatocyte proliferation. We sought to determine the functional role of immune cells, especially NKT cells, in response to partial hepatectomy (PH), and to uncover the impact of the integrin lymphocyte function-associated antigen-1 (LFA-1) on liver regeneration in a subseptic setting.

Methods: Wild-type (WT) and LFA-1-/- mice underwent a 2/3 PH and low-dose lipopolysaccharid (LPS) application. Hepatocyte proliferation, immune cell infiltration, and cytokine profile in the liver parenchyma were determined.

Results: Low-dose LPS application after PH results in a significant delay of liver regeneration between 48h and 72h, which is associated with a reduced number of CD3+ cells within the regenerating liver. In absence of LFA-1, an impaired regenerative capacity was observed under low-dose LPS application. Analysis of different leukocyte subpopulations showed less CD3+NK1.1+ NKT cells in the liver parenchyma of LFA-1-/- mice after PH and LPS application compared to WT controls, while CD3-NK1.1+ NK cells markedly increased. Concordantly with this observation, lower levels of NKT cell related cytokines IL-12 and IL-23 were expressed in the regenerating liver of LFA-1-/- mice, while the expression of NK cell-associated CCL5 and IL-10 was increased compared to WT mice.

Conclusion: A subseptic situation negatively alters hepatocyte proliferation. Within this scenario, we suggest an important impact of NKT cells and postulate a critical function for LFA-1 during processes of liver regeneration.

MeSH terms

  • Animals
  • Cells, Cultured
  • Inflammation / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology
  • Liver / drug effects
  • Liver / metabolism
  • Liver Regeneration / genetics
  • Liver Regeneration / physiology*
  • Lymphocyte Function-Associated Antigen-1 / genetics
  • Lymphocyte Function-Associated Antigen-1 / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Natural Killer T-Cells / metabolism*
  • Natural Killer T-Cells / physiology
  • Parenchymal Tissue / drug effects
  • Parenchymal Tissue / metabolism
  • Phosphorylation / drug effects
  • Phosphorylation / genetics
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Suppressor of Cytokine Signaling 3 Protein / genetics
  • Suppressor of Cytokine Signaling 3 Protein / metabolism

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • Lymphocyte Function-Associated Antigen-1
  • STAT3 Transcription Factor
  • Socs3 protein, mouse
  • Suppressor of Cytokine Signaling 3 Protein

Grants and funding

M.L. received a grant from the Deutsche Forschungsgemeinschaft DFG (SFB 914, project A4) D.H. and N.H. have received a grant from the Gesellschaft für Gastroenterologie in Bayern e.V. Andreas Bolzer is employed by Carl Zeiss Microscopy, ZEISS group. Carl Zeiss Microscopy, ZEISS group provided support in the form of salary for author AB, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific role of this author is articulated in the ‘author contributions’ section