Abstract
Objectives:
Immunologic reactions to antigens released by Aspergillus fumigatus can cause infections such as allergic bronchopulmonary aspergillosis (ABPA). The mucosal surface of the respiratory tract provides host defense mechanism. The aim of this study was to investigate whether respiratory epithelial cells recognize A. fumigatus extract (AE) and initiate an immune response. We report inhibition of Th1 biased epithelial inflammation by an Aspergillus extract.
Methods:
BEAS-2B epithelial cells were cultured in a 37°C incubator in media supplemented with 5% FBS. Cells were treated in duplicate with AE for 1 hour and were stimulated with the TLR3 activator dsRNA for 6 hours. RNA was isolated and was reverse transcribed to cDNA. Realtime polymerase chain reaction analysis was performed in the presence of specific primers and fluorescently labeled probes.
Results:
IFN-β and dsRNA both induced IP-10 mRNA expression in BEAS-2B cells (IFN-β 1081-fold; n = 3; P < .001) (dsRNA 3044-fold; n = 3; P < .001). When BEAS-2B cells were pretreated with AE for 1 hour and then stimulated with IFN-β or dsRNA for 6 hours, induction of IP-10 mRNA was suppressed relative to levels produced by IFN-β and dsRNA alone. Suppressive effects increased with increasing AE concentration. IP-10 protein was induced by IFN-β (control [undetectable] vs IFN-β treated [16.6 ± 9.5 pg/mL] at 6 hours) and by dsRNA (control [undetectable] vs dsRNA [25.3 ± 6.9 pg/mL], at 6 hours, n = 3). We observed significant suppression of IP-10 protein when cells were treated with 1:320 W/V AE concentration (16.6 ± 9.5 pg/mL control vs 2.4 ± 0.25 pg/mL AE treated: P = .005, n = 3).
Conclusions:
We found that AE inhibits the IP-10 mRNA and protein secretion in bronchial epithelial cells.
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