RENAL SYNTHESIS OF LEUKAEMIA INHIBITORY FACTOR (LIF), UNDER NORMAL AND INFLAMMATORY CONDITIONS
Cytokine. 2000-03-01; 12(3): 265-271
DOI: 10.1006/cyto.1999.0545
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1. Cytokine. 2000 Mar;12(3):265-71. doi: 10.1006/cyto.1999.0545.
Renal synthesis of leukaemia inhibitory factor (LIF), under normal and
inflammatory conditions.
Morel DS(1), Taupin JL, Potier M, Deminière C, Potaux L, Gualde N, Moreau JF.
Author information:
(1)Department of Nephrology and Kidney Transplant, Hôpital Pellegrin, Bordeaux,
France.
Leukaemia inhibitory factor (LIF) is a pleiotropic cytokine that is particularly
involved in nephrogenesis and repair of the extracellular matrix. Transgenic
mice overexpressing LIF have mesangial proliferative glomerulonephritis. Also,
during local inflammatory reactions, such as kidney graft rejection or urinary
tract infections, urinary LIF excretion is enhanced. The aim of the study
therefore was to study LIF production by normal and inflammatory diseased
kidneys (glomerulonephritis or graft rejection), maintained in short cultures.
To determine the responsibility of the kidney itself in LIF synthesis, we
measured LIF secretion into the culture supernatants of human mesangial or renal
tubular epithelial cells. Fragments from diseased kidneys, whether grafts or
not, released more LIF than normal human kidney fragments, mesangial or renal
tubular epithelial cells. However, LIF production was delayed in renal
transplants compared to glomerulonephritic samples taken from untreated
patients. In every case, LIF production was enhanced by interleukin 1beta
(IL-1beta) and inhibited by IL-4 or dexamethasone, except in two severe
rejection episodes. So, LIF appeared to respond to pro- and anti-inflammatory
stimuli, in vitro and in vivo. Considering its biological effects, LIF could
play a role in inflammatory renal diseases.
Copyright 2000 Academic Press.
DOI: 10.1006/cyto.1999.0545
PMID: 10704254 [Indexed for MEDLINE]