The reversed passive Arthus reaction as a model for investigating the mechanisms of inflammation-associated hemostasis

Platelets. 2020 May 18;31(4):455-460. doi: 10.1080/09537104.2020.1732325. Epub 2020 Feb 27.


In recent years, accumulating evidence has indicated that platelets continuously repair vascular damage at sites of inflammation and/or infection. Studies in mouse models of inflammation have highlighted the fact that the mechanisms underlying bleeding prevention by platelets in inflamed organs can substantially differ from those supporting primary hemostasis following tail tip transection or thrombus formation in models of thrombosis. As a consequence, exploration of the hemostatic function of platelets in inflammation, as well as assessment of the risk of inflammation-induced bleeding associated with a platelet deficit and/or the use of anti-thrombotic drugs, require the use of dedicated experimental models. In the present review, we present the pros and cons of the cutaneous reversed passive Arthus reaction, a model of inflammation which has been instrumental in studying how inflammation causes vascular injury and how platelets continuously intervene to repair it. The limitations and common issues encountered when working with mouse models of inflammation for investigating platelet functions in inflammation are also discussed.

Keywords: Inflammation; platelets; reversed passive Arthus reaction; vascular integrity.

Publication types

  • Review

MeSH terms

  • Animals
  • Arthus Reaction / drug therapy
  • Arthus Reaction / genetics
  • Arthus Reaction / immunology*
  • Arthus Reaction / physiopathology
  • Blood Platelets / enzymology
  • Blood Platelets / immunology
  • Blood Platelets / metabolism*
  • Blood Platelets / pathology
  • Disease Models, Animal
  • Hemorrhage / immunology
  • Hemorrhage / pathology
  • Hemostasis / drug effects
  • Hemostasis / genetics
  • Hemostasis / immunology*
  • Inflammation / drug therapy
  • Inflammation / genetics
  • Inflammation / immunology*
  • Mice
  • Thrombosis / drug therapy
  • Thrombosis / genetics
  • Thrombosis / physiopathology