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1 Respiratory Section, Edinburgh Lung and The Environment Group Initiative/Colt Laboratories, Department of Medical and Radiological Sciences, The University of Edinburgh Medical School, Edinburgh EH8 9AG; 3 School of Life Sciences, Napier University, Edinburgh EH10 5DT, United Kingdom; and 2 Pulmonary Research Laboratory, St. Pauls' Hospital, The University of British Columbia, Vancouver, British Columbia V6Z 146, Canada
The
presence of the adenoviral early region 1A (E1A) protein in human lungs
has been associated with an increased risk of chronic obstructive
pulmonary disease (COPD), possibly by a mechanism involving
amplification of proinflammatory responses. We hypothesize that
enhanced inflammation results from increased transcription factor
activation in E1A-carrying cells, which may afford susceptibility to
environmental particulate matter < 10 µm
(PM10)-mediated oxidative stress. We measured interleukin
(IL)-8 mRNA expression and protein release in human alveolar epithelial
cells (A549) transfected with the E1A gene (E1A+ve). Both E1A+ve and
ve cells released IL-8 after incubation with TNF-
, but only E1A+ve
cells were sensitive to LPS stimulation in IL-8 mRNA expression and
protein release. E1A+ve cells showed an enhanced IL-8 mRNA and protein
response after treatment with H2O2 and
PM10. E1A-enhanced induction of IL-8 was accompanied by
increases in activator protein-1 and nuclear factor-
B nuclear
binding in E1A+ve cells, which also showed higher basal nuclear binding
of these transcription factors. These data suggest that the presence of
E1A primes the cell transcriptional machinery for oxidative stress
signaling and therefore facilitates amplification of proinflammatory
responses. By this mechanism, susceptibility to exacerbation of COPD in
response to particulate air pollution may occur in individuals
harboring E1A.
early region 1A; environmental particulate matter less than 10 micrometers; interleukin-8; nuclear factor-B; activator protein-1; lung epithelium
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