Lung epithelial cell released nitric oxide protects against pmn
mediated cell injury.
Su, Wei-Yi, Brian J. Day, Bor-Hwang Kang, James D. Crapo, Yuh-Chin T.
Huang, and Ling-Yi Chang.
Department of Medicine, Duke University, Durham, North Carolina
APStracts 3:0097L, 1996.
A calcium-independent Type II nitric oxide synthase (iNOS) has been
localized in lung epithelial cells, however the function of NO x
released by epithelial cells is unclear. We hypothesize that
epithelial derived nitric oxide may affect the interactions between
PMN, the alveolar epithelium and studied PMN adhesion and
cytotoxicity to lung epithelial cells. A dose and time dependent
production of NO x by L-2 cells can be induced by a mixture of
inflammatory mediators (cytomix) containing LPS, TNF[alpha] and
IFN[delta]. Increased NO x production by L-2 cells was associated
with decreased Cr51 release by the epithelial cells after they were
incubated with activated PMNs. Addition of L-NMMA or oxyhemoglobin
reversed the protective effects of cytomix, suggesting that increased
NO x production by L-2 cells was responsible for the decreased Cr51
release. However, PMN adhesion and ICAM-1, a major adhesion molecule
involved in PMN adhesion to epithelium, were increased by cytomix. We
conclude that NO x released by lung epithelial cells was involved in
protecting epithelial cells from PMN mediated cytotoxicity. NO x
mediated protection of lung epithelial cells occurred in spite of PMN
adhesion being increased suggesting that reduced adhesion is not
required for NO x mediated inhibition of PMN cytotoxicity.
Received 28 June 1995; accepted in final form 24 March 1996.
APS Manuscript Number L201-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96