Studies of human respiratory tract inflammation have traditionally relied on the analysis of samples of airway and alveolar lining fluid and bronchial tissue obtained by bronchoscopy. Although the analysis of these samples has contributed much to our current understanding of various pulmonary disease processes, bronchoscopy is invasive, technically difficult, and not always acceptable to volunteer subjects.
Sputum induction (SI) has been demonstrated to be a noninvasive alternate method of assessing airway inflammation that is reproducible, valid, and responsive to changes induced by proinflammatory and antiinflammatory stimuli. While both SI and bronchoscopy appear to be valid methods for assessing airway inflammation, it is not clear whether the results obtained by these two different methods have the same biological meaning. It has been shown that similar qualitative information may be obtained from both induced sputum and bronchoscopy samples (ie, bronchial wash and BAL fluid) in both asthmatic and healthy subjects. Changes in inflammatory cells and mediators in samples of induced sputum also have been shown to be qualitatively similar to those reported in BAL fluid after aerosolized whole-lung allergen challenge and after ozone (O3) exposure. Cell differential counts in induced sputum also have been compared with those in bronchial wash and BAL fluid samples before and after therapy with inhaled corticosteroids (ICSs) or (3-agonists in asthmatic subjects. To our knowledge, however, no direct quantitative comparisons have been performed to demonstrate the degree of association between the changes in inflammatory indexes in induced sputum and those in BAL fluid after an experimental protocol.
To determine whether changes in SI and BAL indexes of airway inflammation are predictive of each other, we performed a randomized crossover study in which asthmatic subjects were exposed either to O3 or filtered air (FA). The respiratory tract lining fluid (RTLF) was then sampled using both SI and bronchoscopy. We then compared the indexes of inflammation in bronchial wash or BAL fluid samples after O3 and FA exposures with those in induced sputum samples.
We chose O3 as the experimental treatment in this study because it produces a significant neutrophilia in airway and alveolar lining fluid, which is readily measurable in induced sputum samples and bronchial wash or BAL fluid samples. We chose to study asthmatic subjects because we and others have previously shown that O3 causes greater airway inflammation in asthmatic subjects compared to healthy subjects.
Read about these reaserches in our forthcoming posts – https://onlineasthmainhalers.com/category/asthma.