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Potentiation of leukotriene production following sequestration of
neutrophils in isolated lungs: indirect evidence for intercellular
leukotriene A4 transfer
F Grimminger, M Menger, G Becker and W Seeger
Department of Internal Medicine, Justus-Liebig-University, Giessen, FRG.
Granulocyte (polymorphonuclear leukocyte, PMN) sequestration in the
microvascular bed with release of different mediators has been implicated
in the pathogenesis of inflammatory and allergic disorders in many organs
including the lung. In the present study, we investigated the profile and
quantity of leukotriene (LT) generation in isolated blood-free perfused
rabbit lungs, in isolated PMNs in vitro and in rabbit lungs, following
administration of PMNs, mimicking pulmonary leukostasis. Following
stimulation with increasing concentrations of the calcium ionophore A 23137
(0.1 to 2 mumol/L), LTs were detected in the buffer fluid by their
chromatographic mobility in different high-performance liquid
chromatography (HPLC) systems, by on- line peak spectrum analysis, and by
post-HPLC radioimmunoassay (RIA). In isolated lungs, a dose-dependent
generation of cysteinyl LTs greater than LTB4, in the complete absence of
omega-oxidation products of LTB4 as well as nonenzymatic hydrolysis
products of LTA4, was evoked. PMNs in vitro showed a typical profile of LT
liberation (LTB4, 20-OH-, and COOH-LTB4, nonenzymatic LTA4 metabolites). In
the model of pulmonary leukostasis, the presence of omega-oxidation
products of LTB4 indicated metabolic integrity of the trapped PMNs.
Nonenzymatic hydrolysis products of LTA4 were, however, not detected in the
combined system, whereas the cysteinyl LTs increased markedly. This profile
suggests intercellular transfer of PMN-derived LTA4 to lung cells in the
microenvironment. In addition, at 2 mumol/L A23187, the sum of all LTA4-
derived products surpassed the arithmetic sum of the isolated preparations
more than threefold. This potentiation of an LT generation under conditions
of pulmonary leukostasis may be of biologic significance for amplification
of inflammatory events.
Volume 72,
Issue 5,
pp. 1687-1692,
11/01/1988
Copyright © 1988 by The American Society of Hematology
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