Project: Research project

Project Details



Exposure to nitrogen dioxide (NO2) is characterized by rapidly increasing
levels of inflammatory mediators and inflammatory cells. There is also a
rapid inhibition of the surface active properties of surfactant and changes
in the levels and nature of some surfactant components, including increased
levels of surfactant-associated protein-A (SP-A). The central hypothesis of
this proposal is that exposure to NO2 causes changes in surfactant and its
constituents, including SP-A. These changes then trigger and enhance
inflammation, causing functional and structural changes that can result in
or contribute to pulmonary disease. In addition, the ability of SP-A to
increase production of reactive oxidant species may contribute to the
inflammatory state resulting from the initial exposure to NO2. The
mechanism(s) responsible for these actions will be investigated by analyzing
the composition of surfactant subfractions and their constituents after
exposure to NO2. The treated surfactant constituents will then be tested
for their ability to modulate TNF-alpha and IL-8 protein and mRNA production
by a macrophage cell line. These will be measured by ELISA and mRNA dot
blotting. The direct effect of NO2 on these cells will then be assessed by
exposing the cells to NO2 and measuring their production of TNF-alpha and
IL-8 in response to other inflammatory stimuli.
Effective start/end date9/30/978/31/99


  • National Heart, Lung, and Blood Institute


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