Disruption of Neutrophil Extracellular Traps (NETs) Links Mechanical Strain to Post-traumatic Inflammation.
Journal: 2019/November - Frontiers in Immunology
ISSN: 1664-3224
Abstract:
Inflammation after trauma is both critical to normal wound healing and may be highly detrimental when prolonged or unchecked with the potential to impair physiologic healing and promote de novo pathology. Mechanical strain after trauma is associated with impaired wound healing and increased inflammation. The exact mechanisms behind this are not fully elucidated. Neutrophil extracellular traps (NETs), a component of the neutrophil response to trauma, are implicated in a range of pro-inflammatory conditions. In the current study, we evaluated their role in linking movement and inflammation. We found that a link exists between the disruption and amplification of NETs which harbors the potential to regulate the wound's response to mechanical strain, while leaving the initial inflammatory signal necessary for physiologic wound healing intact.
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Front Immunol 10: 2148

Disruption of Neutrophil Extracellular Traps (NETs) Links Mechanical Strain to Post-traumatic Inflammation

+10 authors
Click here for additional data file.(3.1M, PDF)
Department of Surgery, University of Michigan Medical School, Ann Arbor, MI, United States
Department of Medicine, University of Michigan Medical School, Ann Arbor, MI, United States
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, United States
Department of Biologic and Materials Sciences & Prosthodontics, University of Michigan School of Dentistry, Ann Arbor, MI, United States
Edited by: Francesca Granucci, University of Milano Bicocca, Italy
Reviewed by: Carmelo Carmona-Rivera, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), United States; Christian Jan Lood, University of Washington, United States
*Correspondence: Benjamin Levi moc.liamg@dmivelneb
This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology
†These authors have contributed equally to this work
Edited by: Francesca Granucci, University of Milano Bicocca, Italy
Reviewed by: Carmelo Carmona-Rivera, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), United States; Christian Jan Lood, University of Washington, United States
Received 2019 Jan 23; Accepted 2019 Aug 27.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Abstract

Inflammation after trauma is both critical to normal wound healing and may be highly detrimental when prolonged or unchecked with the potential to impair physiologic healing and promote de novo pathology. Mechanical strain after trauma is associated with impaired wound healing and increased inflammation. The exact mechanisms behind this are not fully elucidated. Neutrophil extracellular traps (NETs), a component of the neutrophil response to trauma, are implicated in a range of pro-inflammatory conditions. In the current study, we evaluated their role in linking movement and inflammation. We found that a link exists between the disruption and amplification of NETs which harbors the potential to regulate the wound's response to mechanical strain, while leaving the initial inflammatory signal necessary for physiologic wound healing intact.

Keywords: neutrophils, NET, trauma, movement, inflammation
Abstract

Footnotes

Funding. SA funded by NIH F32 {"type":"entrez-nucleotide","attrs":{"text":"AR066499","term_id":"5996715","term_text":"AR066499"}}AR066499, NIH Loan Repayment Program; SJL funded by Howard Hughes Medical Institute (HHMI) Medical Fellows Program; BL funded by NIH, NIGMS K08GM109105, NIH R01GM123069, ACS Clowes Award, International Fibrodysplasia Ossificans Progressiva Association Research Award. JK funded by NIH R01HL134846. YM funded by NIH R01DE020843, DoD W81XWH-11-2-0073.

Footnotes
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