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Curr Opin Immunol. 2018 Dec;55:44-53. doi: 10.1016/j.coi.2018.09.005. Epub 2018 Sep 27.

Coagulopathies and inflammatory diseases: '…glimpse of a Snark'.

Author information

1
Department of Immunobiology, School of Medicine, Yale University, 300 Cedar Street, New Haven, CT 06520, United States.
2
Department of Medicine, School of Medicine, University of Minnesota, 401 East River Parkway, Minneapolis, MN 55455, United States.
3
Department of Neurology, School of Medicine, Yale University, 15 York Street, New Haven, CT 06510, United States; Department of Pharmacology, School of Medicine, Yale University, 333 Cedar Street, New Haven, CT 06520, United States. Electronic address: sourav.ghosh@yale.edu.
4
Department of Immunobiology, School of Medicine, Yale University, 300 Cedar Street, New Haven, CT 06520, United States; Department of Pharmacology, School of Medicine, Yale University, 333 Cedar Street, New Haven, CT 06520, United States. Electronic address: carla.rothlin@yale.edu.

Abstract

Coagulopathies and inflammatory diseases, ostensibly, have distinct underlying molecular bases. Notwithstanding, both are host defense mechanisms to physical injury. In invertebrates, clotting can function directly in anti-pathogen defense. Molecules of the vertebrate clotting cascade have also been directly linked to the regulation of inflammation. We posit that thrombophilia may provide resistance against pathogens in vertebrates. The selective pressure of improved anti-pathogen defense may have retained mutations associated with a thrombophilic state in the human population and directly contributed to enhanced inflammation. Indeed, in some inflammatory diseases, at least a subset of patients can be identified as hypercoagulable. Therefore, anticoagulants such as warfarin or apixaban may have a therapeutic role in some inflammatory diseases.

PMID:
30268838
PMCID:
PMC6366937
[Available on 2019-12-01]
DOI:
10.1016/j.coi.2018.09.005

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