Protective effect of substance p on permeability of airway
epithelial cells in culture.
Yu, Xiao-Ying, Bradley J. Undem, and Ernst Wm. Spannhake.
Department of Environmental Health Sciences, The Johns Hopkins
School of Hygiene and Public Health and Department of Medicine, The
Johns Hopkins School of Medicine
APStracts 3:0136L, 1996.
Although substance P (SP) has been shown to mediate microvascular
leakage in response to various stimuli, some data suggest that, in
contrast, SP may play a protective role in the maintenance of airway
epithelial integrity. To investigate the effect of SP on epithelial
barrier function, we measured paracellular mannitol flux and the
transepithelial potential difference (PD) of human bronchial
epithelial (HBE) and canine bronchial epithelial (CBE) cells.
Incubation of confluent cell cultures with SP had no effect on
baseline flux. However, pretreatment inhibited the flux-enhancing
effects of 0.5 ppm ozone by 50% in HBE cells and 40% in CBE cells,
and inhibited the ozone-induced decrease in PD in CBE cells by 54%.
SP-afforded protection was reduced by the NK-1 receptor antagonist,
CP- 96,345. NK-1 and NK-3 receptor agonists also inhibited ozone
-induced permeability, whereas an NK-2 receptor agonist was without
significant effect. These data indicate that SP exerts a protective
effect on bronchial epithelial barrier function under conditions of
challenge, which appears to be mediated in large part through NK-1
receptors.
Received 25 August 1995; accepted in final form 26 July 1996.
APS Manuscript Number L259-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996