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1 Department of Pulmonary Medicine, 2 Institute for Experimental Medical Research, and 3 Research Forum, Ullevål Hospital, University of Oslo, 0407 Oslo, Norway
Endothelin (ET)-1 has been
launched as an important mediator in bronchial asthma, which is an
eosinophilic airway inflammation. However, the interplay between ET-1
and other proinflammatory mediators during the development of airway
inflammation has not been elucidated. We wanted to study 1)
whether the production of ET-1 precedes the production of other
proinflammatory mediators and 2) whether ET-1 stimulates the
production of these mediators within the airways. These hypotheses were
studied during the development of an eosinophilic airway inflammation
in rats. The increase in ET-1 mRNA level in lung tissue preceded the
increase in mRNA levels of tumor necrosis factor-
, interleukin
(IL)-1
, and IL-8. Treatment of the animals with the ET receptor
antagonist bosentan resulted in a substantial decrease in the
concentrations of tumor necrosis factor-, IL-4, IL-1,
interferon-
, and ET-1 in bronchoalveolar lavage fluid. In
conclusion, the synthesis of ET-1 as measured by increased mRNA level
precedes the synthesis of other proinflammatory cytokines of importance
for the development of an eosinophilic airway inflammation, and ET
antagonism inhibits the production of these mediators within the
airways. Whether treatment with ET antagonists will prove beneficial
for patients with eosinophilic airway inflammations like bronchial
asthma is not yet known.
asthma
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