Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Author:

Ekdahl Kristina N.12,Teramura Yuji13,Hamad Osama A.1,Asif Sana1,Duehrkop Claudia1,Fromell Karin1,Gustafson Elisabet4,Hong Jaan1,Kozarcanin Huda1,Magnusson Peetra U.1,Huber‐Lang Markus5,Garred Peter6,Nilsson Bo1

Affiliation:

1. Department of Immunology, Genetics and Pathology (IGP) Rudbeck Laboratory C5:3 Uppsala University Uppsala Sweden

2. Linnæus Center of Biomaterials Chemistry Linnæus University Kalmar Sweden

3. Department of Bioengineering The University of Tokyo Tokyo Japan

4. Department of Women's and Children's Health Uppsala University Hospital Uppsala Sweden

5. Department of Orthopedic Trauma, Hand, Plastic and Reconstructive Surgery University of Ulm Ulm Germany

6. Laboratory of Molecular Medicine Department of Clinical Immunology Section 7631 Faculty of Health and Medical Sciences Rigshospitalet University of Copenhagen Copenhagen Denmark

Abstract

SummaryInnate immunity is fundamental to our defense against microorganisms. Physiologically, the intravascular innate immune system acts as a purging system that identifies and removes foreign substances leading to thromboinflammatory responses, tissue remodeling, and repair. It is also a key contributor to the adverse effects observed in many diseases and therapies involving biomaterials and therapeutic cells/organs. The intravascular innate immune system consists of the cascade systems of the blood (the complement, contact, coagulation, and fibrinolytic systems), the blood cells (polymorphonuclear cells, monocytes, platelets), and the endothelial cell lining of the vessels. Activation of the intravascular innate immune system in vivo leads to thromboinflammation that can be activated by several of the system's pathways and that initiates repair after tissue damage and leads to adverse reactions in several disorders and treatment modalities. In this review, we summarize the current knowledge in the field and discuss the obstacles that exist in order to study the cross‐talk between the components of the intravascular innate immune system. These include the use of purified in vitro systems, animal models and various types of anticoagulants. In order to avoid some of these obstacles we have developed specialized human whole blood models that allow investigation of the cross‐talk between the various cascade systems and the blood cells. We in particular stress that platelets are involved in these interactions and that the lectin pathway of the complement system is an emerging part of innate immunity that interacts with the contact/coagulation system. Understanding the resulting thromboinflammation will allow development of new therapeutic modalities.

Funder

Vetenskapsrådet

Seventh Framework Programme

Swedish Foundation for International Cooperation in Research and Higher Education

Japan Society for the Promotion of Science

Linnéuniversitetet

Publisher

Wiley

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