title: Both IL-1β and TNF-α regulate NGAL expression in polymorphonuclear granulocytes of chronic hemodialysis patients.
abstract: BACKGROUND
  NGAL is involved in modulation of the inflammatory response and is found in the sera of uremic patients. We investigated whether hemodiafiltration (HDF) could influence the ability of polymorphonuclear granulocytes (PMGs) to release NGAL. The involvement of interleukin- (IL-)1β and tumor necrosis factor- (TNF-)α on NGAL release was evaluated.
  
  
  METHODS
  We studied end-stage renal disease (ESRD) patients at the start of dialysis (Pre-HDF) and at the end of treatment (Post-HDF) and 18 healthy subjects (HSs). Peripheral venous blood was taken from HDF patients at the start of dialysis and at the end of treatment.
  
  
  RESULTS
  PMGs obtained from ESRD patients were hyporesponsive to LPS treatment, with respect to PMG from HS. IL-1β and TNF-α produced by PMG from post-HDF patients were higher than those obtained by PMG from pre-HDF. Neutralization of IL-1β, but not of TNF-α, determined a clear-cut production of NGAL in PMG from healthy donors. On the contrary, specific induction of NGAL in PMG from uremic patients was dependent on the presence in supernatants of IL-1β and TNF-α.
  
  
  CONCLUSIONS
  Our data demonstrate that in PMG from healthy subjects, NGAL production was supported solely by IL-1β, whereas in PMG from HDF patients, NGAL production was supported by IL-1β, TNF-α.
authors.affiliation: Unit of Clinical Microbiology, Department of Surgical Science, Faculty of Medicine, University of Messina, 98125 Messina, Italy.
authors.forename: Adriana
authors.initials: A
authors.lastname: Arena
authors.forename: Giovanna
authors.initials: G
authors.lastname: Stassi
authors.forename: Daniela
authors.initials: D
authors.lastname: Iannello
authors.forename: Domenica
authors.initials: D
authors.lastname: Gazzara
authors.forename: Maria
authors.initials: M
authors.lastname: Calapai
authors.forename: Carlo
authors.initials: C
authors.lastname: Bisignano
authors.forename: Davide
authors.initials: D
authors.lastname: Bolignano
authors.forename: Antonio
authors.initials: A
authors.lastname: Lacquaniti
authors.forename: Michele
authors.initials: M
authors.lastname: Buemi
mesh_terms: D000209:Acute-Phase Proteins; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D057134:Antibodies, Neutralizing; D016022:Case-Control Studies; D005260:Female; D017583:Hemodiafiltration; D006801:Humans; D007113:Immunity, Innate; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000097:blood; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000276:immunology / Q000628:therapy; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000097:blood*
chemical_list: D000209:Acute-Phase Proteins; D000911:Antibodies, Monoclonal; D057134:Antibodies, Neutralizing; D018836:Inflammation Mediators; D053583:Interleukin-1beta; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D014409:Tumor Necrosis Factor-alpha