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Effect of ozone and nitrogen dioxide on the permeability of bronchial epithelial cell cultures of non‐asthmatic and asthmatic subjects
Author(s) -
Bayram H.,
Rusznak C.,
Khair O. A.,
Sapsford R. J.,
Abdelaziz M. M.
Publication year - 2002
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1046/j.1365-2745.2002.01435.x
Subject(s) - asthma , immunology , medicine , ozone , in vivo , nitrogen dioxide , chemistry , biology , microbiology and biotechnology , organic chemistry
Summary Background Although epidemiological as well as in vivo exposure studies suggest that ozone (O 3 ) and nitrogen dioxide (NO 2 ) may play a role in airway diseases such as asthma, the underlying mechanisms are not clear. Objective Our aim was to investigate the effect of O 3 and NO 2 on the permeability of human bronchial epithelial cell (HBEC) cultures obtained from non‐atopic non‐asthmatic (non‐asthmatics) and atopic mild asthmatic (asthmatics) individuals. Methods We cultured HBECs from bronchial biopsies of non‐asthmatics and asthmatics, and exposed these for 6 h to air, 10 to 100 parts per billion (p.p.b.) O 3 , or to 100 to 400 p.p.b. NO 2 , and assessed changes in electrical resistance (ER) and movement of 14C‐BSA across the cell cultures. Results Although exposure to either O 3 or NO 2 did not alter the permeability of HBEC cultures of non‐asthmatics, 10 to 100 p.p.b. O 3 and 400 p.p.b. NO 2 significantly decreased the ER of HBEC cultures of asthmatics, when compared with exposure to air. Additionally, 10, 50 and 100 p.p.b. O 3 led to a significant increase in the movement of 14C‐BSA across asthmatic HBEC cultures, after 6 h of exposure (medians = 1.73%; P < 0.01, 1.50%; P < 0.05 and 1.53%, P < 0.05, respectively), compared with air exposed cultures (median = 0.89%). Similarly, exposure for 6 h to both 200 and 400 p.p.b. NO 2 significantly increased the movement of 14C‐BSA across asthmatic HBEC cultures, when compared with air exposure. A comparison of data obtained from the two study groups demonstrated that 10 to 100 p.p.b. O 3 ‐ and 200 to 400 p.p.b. NO 2 ‐induced epithelial permeability was greater in cultures of asthmatics compared with non‐asthmatics. Conclusion These results suggest that HBECs of asthmatics may be more susceptible to the deleterious effects of these pollutants. Whether in patients with asthma the greater susceptibility of bronchial epithelial cells to O 3 and NO 2 contributes to the development of the disease, or is a secondary characteristic of this condition, remains to be determined.