URINARY TRYPSIN-INHIBITOR REDUCES THE RELEASE OF HISTAMINE FROM RAT PERITONEAL MAST-CELLS

Citation
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
ISSN journal
0022-2143
Volume
131
Issue
4
Year of publication
1998
Pages
375 - 385
Database
ISI
SICI code
0022-2143(1998)131:4<375:UTRTRO>2.0.ZU;2-R
Abstract
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.