Endotoxin stimulates the expression of group ii phospholipase a2 in
rat lung in vivo and in isolated perfused lungs.
Ljungman, Anders G., Christer Tagesson, and Mats Lindahl.
Department of Occupational and Environmental Medicine, Faculty of
Health Sciences, University of Link[diaeresis]oping, S-581 85
Link[diaeresis]oping, Sweden
APStracts 2:0233L, 1995.
Injection of endotoxin in vivo leads to increased phospholipase A2
(PLA2) activity in the lung but the type(s) of PLA2 involved has not
been clarified, nor the importance of blood components and/or
different inflammatory cytokines. In the present study, injection of
endotoxin in rats caused increased lung levels of group II PLA2, TNF
-[alpha] and Il-1[beta] mRNA, while group I PLA2 mRNA levels were
unaffected. The augmented group II PLA2 mRNA levels corresponded to a
rise in membrane-associated PLA2 enzymatic activity that was
inhibited by rutin, an inhibitor of group II PLA2. In blood-free,
salt-perfused lungs, addition of endotoxin to the perfusate caused
elevated group II PLA2, TNF-[alpha] and Il-1[beta] mRNA levels and
release of PLA2 and TNF-[alpha] activity into the perfusate, and when
instilled intratracheally, endotoxin caused increased PLA2 activity
in the lung tissue. It is concluded that; (i) endotoxin stimulates
group II PLA2, but not group I PLA2, in rat lung cells, (ii) this
stimulation is accompanied by increased expression of TNF-[alpha] and
Il-1[beta], and (iii) endotoxin-induced PLA2 activation and cytokine
production in the lung are not dependent on circulating blood
components.
Received 2 September 1994; accepted in final form 28 November
1995.
APS Manuscript Number L260-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95