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Departments of
* Internal Medicine and
Anatomy, Justus-Liebig University, Giessen, Germany
The influence of LPS preincubation on hydrogen peroxide
(H2O2)-induced loss of epithelial barrier
function was investigated in rat alveolar epithelial type II cells
(ATII). Both apical and basolateral H2O2
administration caused a manyfold increase in transepithelial
[3H]mannitol passage. Apical but not basolateral
preincubation of ATII with LPS did not influence control barrier
properties but fully abrogated the H2O2-induced
leakage response. The effect of apical LPS was CD14 dependent and was
accompanied by a strong up-regulation of NO synthase II mRNA and
protein and NO release. Inhibition of NO by
NG-monomethyl-L-arginine
suppressed the LPS effect, whereas it was reproduced by exogenous
application of gaseous NO or NO donor agents. Manipulation of the
glutathione homeostasis
(buthionine-(S,R)-sulfoximine) and the
cGMP pathway (1H-(1,2,4)oxadiazolo[4,3-
]quinoxaline-1-one;
zaprinast) did not interfere with the protective effect of LPS.
Superoxide (O
2) generation by ATII cells was reduced by
exogenous NO and LPS preincubation. O2 scavenging with
exogenous superoxide dismutase, the intracellular superoxide
dismutase analog Mn(III)tetrakis(4-benzoic acid) porphyrin, and the
superoxide scavenger nitroblue tetrazolium and, in particular, hydroxyl
radical scavenging with hydroxyl radical scavenger
1,3-dimethyl-thiourea inhibited the
H2O2-induced epithelial leakage response. In
conclusion, apical but not basolateral LPS preincubation of ATII cells
provides strong protection against H2O2-induced
transepithelial leakage, attributable to an up-regulation of epithelial
NO synthesis. It is suggested that the LPS-induced NO formation is
effective via interaction with reactive oxygen species, including
superoxide and hydroxyl radicals. The polarized epithelial response to
LPS may be part of the lung innate immune system, activated by inhaled
endotoxin or under conditions of pneumonia.
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