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Leukotrienes B 4 and C 4 in MS
Author(s) -
Prosiegel M.,
Ned I.,
Wildfeuer A.,
Mehlber L.,
Mallinger J.,
RuhenstrothBauer G.
Publication year - 1987
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1987.tb05460.x
Subject(s) - leukotriene c4 , leukotriene , leukotriene b4 , platelet , ionophore , multiple sclerosis , intracellular , stimulation , chemistry , arachidonate 5 lipoxygenase , granulocyte , neutrophile , immunology , medicine , endocrinology , inflammation , biochemistry , arachidonic acid , membrane , enzyme , asthma
Release of leukotriene B 4 (LTB 4 ) and leukotriene C 4 (LTC 4 ) from neutrophils and platelet‐neutrophil suspensions in response to ionophore A23187 was measured in 12 multiple sclerosis (MS) patients and 8 healthy volunteers. LTC 4 release from neutrophils, as well as from platelet‐neutrophil suspensions, was significantly decreased in MS patients compared with the controls. There was no significant difference in the release of LTB 4 between MS patients and controls. The findings suggest that permanent stimulation of platelets and neutrophils e.g., by encephalitogenic peptide leads to continuous LTC 4 release with subsequent depletion of intracellular substrates serving as precursors for the formation of 5‐li‐poxygenase products. Since the target of microvascular actions of LTC 4 are postcapillary venules, the release of this sulfidopeptide leukotriene might play a pathogenetic role in the formation of MS lesions.