Journal
INTERNATIONAL IMMUNOLOGY
Volume 32, Issue 5, Pages 359-368Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxz084
Keywords
enoxaparin; fondaparinux; heparan sulfate; imaging flow cytometry; neutrophil extracellular trap
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Funding
- Japan Society for the Promotion of Science [JP17F17117]
- Japan Agency for Medical Research and Development [AMED J-PRIDE 17fm0208021h0001]
- Japan Science and Technology Agency (JST-CREST)
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Heparin is used extensively as an anticoagulant in a broad range of diseases and procedures; however, its biological effects are not limited to coagulation and remain incompletely understood. Heparin usage can lead to the life-threatening complication known as heparin-induced thrombocytopenia (HIT), caused by the development of antibodies against heparin/PF4 complexes. Here, we demonstrate the ability of heparin to induce neutrophil extracellular traps (NETs). NETs occurred with cell lysis and death, but live neutrophils releasing extracellular DNA strands, known as vital NETs, also occurred abundantly. Formation of NETs was time and dose dependent, and required reactive oxygen species and neutrophil elastase. Other compounds related to heparin such as low molecular weight heparin, fondaparinux and heparan sulfate either failed to induce NETs, or did so to a much lesser extent. Our findings suggest the ability of heparin to directly induce NET formation should be considered in the context of heparin treatment and HIT pathogenesis.
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