Document Detail

Both IL-1β and TNF-α regulate NGAL expression in polymorphonuclear granulocytes of chronic hemodialysis patients.
MedLine Citation:
PMID:  21403867     Owner:  NLM     Status:  MEDLINE    
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.
CONCLUSION: 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.
Adriana Arena; Giovanna Stassi; Daniela Iannello; Domenica Gazzara; Maria Calapai; Carlo Bisignano; Davide Bolignano; Antonio Lacquaniti; Michele Buemi
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Publication Detail:
Type:  In Vitro; Journal Article     Date:  2011-03-03
Journal Detail:
Title:  Mediators of inflammation     Volume:  2010     ISSN:  1466-1861     ISO Abbreviation:  Mediators Inflamm.     Publication Date:  2010  
Date Detail:
Created Date:  2011-03-15     Completed Date:  2011-07-08     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  9209001     Medline TA:  Mediators Inflamm     Country:  United States    
Other Details:
Languages:  eng     Pagination:  613937     Citation Subset:  IM    
Unit of Clinical Microbiology, Department of Surgical Science, Faculty of Medicine, University of Messina, 98125 Messina, Italy.
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MeSH Terms
Acute-Phase Proteins
Antibodies, Monoclonal
Antibodies, Neutralizing
Case-Control Studies
Immunity, Innate
Inflammation Mediators / antagonists & inhibitors,  blood
Interleukin-1beta / antagonists & inhibitors,  blood*
Kidney Failure, Chronic / blood*,  immunology,  therapy
Lipocalins / blood*
Middle Aged
Neutrophils / immunology,  metabolism*
Proto-Oncogene Proteins / blood*
Tumor Necrosis Factor-alpha / antagonists & inhibitors,  blood*
Reg. No./Substance:
0/Acute-Phase Proteins; 0/Antibodies, Monoclonal; 0/Antibodies, Neutralizing; 0/Inflammation Mediators; 0/Interleukin-1beta; 0/LCN2 protein, human; 0/Lipocalins; 0/Proto-Oncogene Proteins; 0/Tumor Necrosis Factor-alpha

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