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The fifth epidermal growth factor like region of thrombomodulin alleviates LPS-induced sepsis through interacting

Bin Pan, Xiangmin Wang, Shinsuke Kojima

  • 1Kailin Xu, MD, Department of Hematology, The Affiliated Hospital of Xuzhou Medical University, #99 West Huaihai Road, Xuzhou 221002, China, Tel.: +86 516 8580 2382, Fax: +86 516 8560 1527,

Thrombosis and Haemostasis
|January 13, 2017
PubMed

Insights

Thrombomodulin

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Thrombomodulin (TM) has known cytoprotective effects via its TME5 domain, interacting with GPR15 on vascular endothelial cells.
  • The anti-inflammatory mechanisms of TM remain largely unknown.
  • Sepsis involves complex inflammation and coagulation dysregulation.

Purpose of the Study:

  • To investigate the role of TME5 in modulating inflammation and coagulation during sepsis.
  • To elucidate the mechanism by which TME5 exerts anti-inflammatory effects.

Main Methods:

  • Utilized a lipopolysaccharide (LPS)-induced murine sepsis model.
  • Assessed the effects of TME5 treatment on sepsis outcomes, inflammation, and coagulation.
  • Confirmed TME5-GPR15 interaction in vitro and evaluated the impact of GPR15 knockout.

Main Results:

  • TME5 treatment ameliorated inflammation and coagulopathy in LPS-induced sepsis.
  • TME5 directly binds to GPR15, and GPR15 knockout abrogated TME5's protective effects.
  • GPR15 mediated TME5's anti-inflammatory action by suppressing NF-κB signaling in macrophages.

Conclusions:

  • TME5 exerts anti-inflammatory effects in sepsis through GPR15-dependent inhibition of NF-κB signaling.
  • GPR15 knockout leads to dysregulated macrophage immune responses.
  • TME5 represents a potential therapeutic strategy for sepsis treatment.
Keywords:
G-protein coupled receptor 15Thrombomodulinlipopolysaccharidemacrophagessepsis

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