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01.12.2015 | Research article | Ausgabe 1/2015 Open Access

BMC Pulmonary Medicine 1/2015

Effects of controlled diesel exhaust exposure on apoptosis and proliferation markers in bronchial epithelium – an in vivo bronchoscopy study on asthmatics, rhinitics and healthy subjects

Zeitschrift:
BMC Pulmonary Medicine > Ausgabe 1/2015
Autoren:
Annelie F Behndig, Karthika Shanmuganathan, Laura Whitmarsh, Nikolai Stenfors, Joanna L Brown, Anthony J Frew, Frank J Kelly, Ian S Mudway, Thomas Sandström, Susan J Wilson
Wichtige Hinweise

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

AFB participated in the design of the study, recruited and screened study subjects, performed the bronchoscopies, drafted and finalised the manuscript. JB supervised the diesel exhaust exposures. KS and LW carried out the immunohistochemistry. AJF, FJK and TS participated in the design of the study. NS participated in the design of the study and performed the bronchoscopies. ISM participated in the design of the study and drafting of the manuscript. SJW conceived of the study, participated in its design and coordination, supervised the IHC work and helped to draft the manuscript. All authors read and approved the final manuscript.

Abstract

Background

Epidemiological evidence demonstrates that exposure to traffic-derived pollution worsens respiratory symptoms in asthmatics, but controlled human exposure studies have failed to provide a mechanism for this effect. Here we investigated whether diesel exhaust (DE) would induce apoptosis or proliferation in the bronchial epithelium in vivo and thus contribute to respiratory symptoms.

Methods

Moderate (n = 16) and mild (n = 16) asthmatics, atopic non-asthmatic controls (rhinitics) (n = 13) and healthy controls (n = 21) were exposed to filtered air or DE (100 μg/m3) for 2 h, on two separate occasions. Bronchial biopsies were taken 18 h post-exposure and immunohistochemically analysed for pro-apoptotic and anti-apoptotic proteins (Bad, Bak, p85 PARP, Fas, Bcl-2) and a marker of proliferation (Ki67). Positive staining was assessed within the epithelium using computerized image analysis.

Results

No evidence of epithelial apoptosis or proliferation was observed in healthy, allergic or asthmatic airways following DE challenge.

Conclusion

In the present study, we investigated whether DE exposure would affect markers of proliferation and apoptosis in the bronchial epithelium of asthmatics, rhinitics and healthy controls, providing a mechanistic basis for the reported increased airway sensitivity in asthmatics to air pollutants. In this first in vivo exposure investigation, we found no evidence of diesel exhaust-induced effects on these processes in the subject groups investigated.
Literatur
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