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Diesel exhaust does not affect apoptosis in the bronchial epithelium in patients with asthma
Diesel exhaust appeared to have no impact on markers of proliferation and apoptosis in the bronchial epithelium in patients with asthma, rhinitis and healthy controls, according to results from a follow-up study.
“In this study, we investigated the hypothesis that diesel exhaust would lead to an increase in apoptosis accompanied by impaired repair reflected by decreased proliferation in the bronchial epithelium of asthmatics, providing a mechanistic basis for their reported increased sensitivity to air pollutants,” Annelie F. Behndig, MD, a senior physician in the department of public health and clinical medicine at Umeå University in Sweden, and colleagues wrote. “Contrary to our hypothesis we found no evidence of the induction of these processes in either mild to moderate asthmatics or allergic rhinitics following diesel exhaust challenge.”
Behndig and colleagues exposed patients with mild (n = 16) to moderate (n = 16) asthma, patients with rhinitis (n = 13) and healthy controls (n = 21) to filtered air or diesel exhaust (100 µg/m3) for 2 hours — on two separate occasions — to analyze if diesel exhaust induced apoptosis or proliferation in the bronchial epithelium in vivo and contribute to respiratory symptoms.
The researchers then collected bronchial biopsies 18 hours after the exposure and analyzed for pro-apoptotic and anti-apoptotic proteins — Bad, Bak, p85, PARP, Fas and Bcl-2 — as well as a marker of proliferation — Ki67.
No evidence of epithelial apoptosis or proliferation appeared to exist in the healthy controls, the patients with asthma or the patients with rhinitis after the challenge.
More research is needed to further explore the interaction between airway response and air pollution, the researchers wrote.
“We acknowledge that this interpretation is limited by the single time point examined, and further studies will be required before we can fully exclude the involvement of these pathways in the induction of airway hyper responsiveness after exposure to particulate matter air pollution,” the researchers wrote. – by Ryan McDonald
Disclosure: The researchers report no relevant financial disclosures.