H. Kobayashi et al., URINARY TRYPSIN-INHIBITOR REDUCES THE RELEASE OF HISTAMINE FROM RAT PERITONEAL MAST-CELLS, The Journal of laboratory and clinical medicine, 131(4), 1998, pp. 375-385
Citations number
52
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medicine, General & Internal","Medicine, Research & Experimental","Medical Laboratory Technology
We determined the ability of urinary trypsin inhibitor (UTI), which is
a Kunitz-type protease inhibitor present in serum and in urine, to in
hibit rat peritoneal mast cell (RPMC) mediator release induced by seve
ral stimuli, UTI attenuated the immunoglobulin E-mediated release of b
oth preformed (histamine) and newly formed (leukotriene C-4,) mediator
s from RPMCs, Inhibition (21% +/- 5%) of the anti-IgE-triggered releas
e of histamine was observed after a 30-minute incubation of RPMCs with
UTI (5 mu mol/L). To investigate the specificity of the UTI effect, w
e studied the stimulatory activity of phorbol ester (phorbol 12-myrist
ate 13-acetate (PMA)) or calcium ionophore A23187 in control and UTI-t
reated mast cells, The efficacy of UTI as an inhibitor was dependent o
n the nature of the stimulus, because histamine release induced by PMA
-mediated or calcium ionophore A23187-mediated processes was not inhib
ited by UTI, A series of structurally distinct protease inhibitors did
not inhibit IgE-induced release of mediators from RPMCs, The Kunitz-t
ype protease inhibitors are important in the regulation of RPMC functi
on. In parallel with the UTI-related decrease in anti-IgE stimulatory
activity on mediator release, increased microviscosity of membrane lip
ids could be observed by two independent experiments on fluorescence p
olarization with diphenylhexatriene (DPH) and on the fluorescence prob
e fluorescein isothiocyanate-concanavalin A. UTI reduces mediator rele
ase by a mechanism-possibly an interruption of the coupling of recepto
r and effector systems-because UTI acts as an agent to decrease biolog
ic lipid membrane fluidity.