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Pancreatectomy Induces Cancer-Promoting Neutrophil Extracellular Traps

Ivey, Abby D. ; Pratt, Hillary G. ; Niemann, Britney ; Ranson, Kristen ; Puleo, Amanda ; Fagan, B. Matthew ; Rao, Pavan ; Landreth, Kaitlyn M. ; Liu, Tracy W. ; Boone, Brian A.

Annals of surgical oncology, 2024-06, Vol.31 (6), p.3707-3717 [Periódico revisado por pares]

Cham: Springer International Publishing

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Título:
Pancreatectomy Induces Cancer-Promoting Neutrophil Extracellular Traps
Autor: Ivey, Abby D. ; Pratt, Hillary G. ; Niemann, Britney ; Ranson, Kristen ; Puleo, Amanda ; Fagan, B. Matthew ; Rao, Pavan ; Landreth, Kaitlyn M. ; Liu, Tracy W. ; Boone, Brian A.
Assuntos: Adult ; Aged ; Biomarkers, Tumor - blood ; Biomarkers, Tumor - metabolism ; Cell-Free Nucleic Acids - blood ; Chromatin ; Citrulline ; Colony-stimulating factor ; Enzyme-linked immunosorbent assay ; Extracellular Traps - metabolism ; Female ; Follow-Up Studies ; Granulocyte colony-stimulating factor ; Granulocyte Colony-Stimulating Factor - blood ; Histone H3 ; Histones ; Histones - blood ; Histones - metabolism ; Humans ; Inflammation ; Interleukin 6 ; Interleukin-6 - blood ; Leukocytes (granulocytic) ; Leukocytes (neutrophilic) ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Neutrophils ; Neutrophils - metabolism ; Neutrophils - pathology ; Oncology ; Pancreas ; Pancreatectomy ; Pancreatectomy - adverse effects ; Pancreatic diseases ; Pancreatic Neoplasms - pathology ; Pancreatic Neoplasms - surgery ; Patients ; Plasma levels ; Postoperative period ; Prognosis ; Prospective Studies ; Retrospective Studies ; Surgery ; Surgical Oncology ; Translational Research ; Wound healing
É parte de: Annals of surgical oncology, 2024-06, Vol.31 (6), p.3707-3717
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Descrição: Background Neutrophil extracellular traps (NETs) occur when neutrophil chromatin is decondensed and extruded into the extracellular space in a web-like structure. Originally described as an anti-microbial function, this process has been implicated in the pathogenesis of pancreatic disease. In addition, NETs are upregulated during physiologic wound-healing and coagulation. This study evaluated how the inflammatory response to pancreatic surgery influences NET formation. Methods For this study, 126 patients undergoing pancreatectomy gave consent before participation. Plasma was collected at several time points (preoperatively and through the postoperative outpatient visit). Plasma levels of NET markers, including cell-free DNA (cfDNA), citrullinated histone H3 (CitH3), interleukin (IL)-8, IL-6, and granulocyte colony-stimulating factor (G-CSF) were measured using enzyme-linked immunosorbent assay (ELISA). Patient clinical data were retrospectively collected from a prospectively maintained database. Results After pancreatic resection, NET markers (cfDNA and CitH3) were elevated, peaking on postoperative days 3 and 4. This increase in NETs was due to an inherent change in neutrophil biology. Postoperatively, NET-inducing cytokines (IL-8, IL-6, and G-CSF) were increased, peaking early in the postoperative course. The patients undergoing the robotic approach had a reduction in NETs during the postoperative period compared with those who underwent the open approach. The patients who experienced a pancreatic leak had an increase in NET markers during the postoperative period. Conclusions Pancreatectomy induces cancer-promoting NET formation. The minimally invasive robotic approach may induce fewer NETs, although the current analysis was limited by selection bias. Pancreatic leak resulted in increased NETs. Further study into the potential for NET inhibition during the perioperative period is warranted.
Editor: Cham: Springer International Publishing
Idioma: Inglês

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Pancreatectomy Induces Cancer-Promoting Neutrophil Extracellular Traps

Ivey, Abby D. ; Pratt, Hillary G. ; Niemann, Britney ; Ranson, Kristen ; Puleo, Amanda ; Fagan, B. Matthew ; Rao, Pavan ; Landreth, Kaitlyn M. ; Liu, Tracy W. ; Boone, Brian A.

Cham: Springer International Publishing

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