title: Cytokine-modulated inhibition of neutrophil apoptosis at local site augments exudative neutrophil functions and reflects inflammatory response after surgery.
abstract: BACKGROUND
  The fate of exudative polymorphonuclear neutrophils (PMNs) at the local site after surgery is not well understood. We evaluated the fate and functions of exudative PMNs at the local site in patients who were undergoing major surgery. We also investigated the relation between PMN apoptosis and cytokine levels at the local site during the postoperative period.
  
  
  METHODS
  Exudative PMNs were isolated from 11 patients during the postoperative period. Apoptosis, reactive oxygen intermediates (ROI) production, CD16, and tumor necrosis factor receptor expression of the PMNs were determined by flow cytometry. Cytokine levels in the drainage fluid were measured.
  
  
  RESULTS
  Exudative PMN apoptosis was markedly inhibited on postoperative day 1 and then increased in a time-dependent manner. IL-6 and granulocyte macrophage colony-stimulating factor were significant factors to inhibit exudative PMN apoptosis; tumor necrosis factor-alpha and IL-10 were the factors to increase apoptosis. ROI production and CD16 expression of exudative PMNs were augmented when PMN apoptosis was inhibited in the early postoperative period.
  
  
  CONCLUSIONS
  Exudative PMN apoptosis was inhibited after surgery; PMN function was augmented after surgery. Cytokines at the local site may modulate exudative PMN apoptosis. Exudative PMN apoptosis reflected the inflammatory response after surgery. Understanding the mechanisms of PMN apoptosis and its pathophysiologic significance at local inflammatory sites in vivo may help in the design of more rational treatments.
authors.affiliation: Department of Surgery I, Surgical Center, University of Tokyo, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Fukatsu
authors.forename: I
authors.initials: I
authors.lastname: Han
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
authors.forename: S
authors.initials: S
authors.lastname: Ikeda
authors.forename: A
authors.initials: A
authors.lastname: Hidemura
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000276:immunology*; D016207:Cytokines / Q000097:blood / Q000378:metabolism*; D005122:Exudates and Transudates / Q000166:cytology / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D008875:Middle Aged; D009504:Neutrophils / Q000166:cytology* / Q000276:immunology* / Q000378:metabolism; D011003:Ploidies; D011183:Postoperative Complications / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D013997:Time Factors
chemical_list: D016207:Cytokines; D017382:Reactive Oxygen Species; D018124:Receptors, Tumor Necrosis Factor