Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.

Endotoxin (Lipopolysaccharide, LPS) is a potent inducer of inflammation and there is various LPS contamination in the environment, being a trigger of lung diseases and exacerbation. The objective of this study was to assess the time course of inflammation and the sensitivities of the airways and alveoli to targeted LPS inhalation in order to understand the role of LPS challenge in airway disease.In healthy volunteers without any bronchial hyperresponsiveness we targeted sequentially 1, 5 and 20 µg LPS to the airways and 5 µg LPS to the alveoli using controlled aerosol bolus inhalation.

Fractionated exhaled breath condensate collection shows high hydrogen peroxide release in the airways.

Background: Exhaled breath condensate (EBC) allows noninvasive monitoring of inflammation in the lung. Activation of inflammatory cells results in an increased production of reactive oxygen species, leading to the formation of hydrogen peroxide (H(2)O(2)). In addition, cigarette smoking causes an influx of inflammatory cells, and higher levels of H(2)O(2) have been found in EBC of smokers.