We aimed to evaluate IDO expression in two well defined human phenotypes: controls and their atopic counter-parts. Skin prick tests (SPT) were performed on all study subjects to confirm diagnosis. The control and atopic groups did not differ in terms of patient number, age, sex, peripheral blood eosinophils, percentage of peripheral blood eosinophils. (p > 0,05 Kruskal-Wallis, Mann Whitney U) In comparison to controls, atopics had significantly higher serum IgE levels as well as significantly higher IgE levels against allergens to which the subjects were allergic. Atopics and controls differed in their symptom score only during the spring (in season, natural allergen exposure). Surprisingly, there were no differences between inflammation score, leukocyte numbers, percentages of eosinophils, IDO+ in epithelial cells and leucocytes during winter (off season) and spring. Atopics had a higher number of eosinophils during spring only.
We observed that in the nasal cavity, expression of IDO was low and did not differ between atopic and non-atopic groups. Moreover IDO expression did not fluctuate in the same individuals between symptomatic spring and asymptomatic winter season. We have also previously shown that the role of the nasal epithelium in birch pollen atopy is important . In contrast others have shown that IDO might have a role in atopy. Paveglio et al. very recently showed in a transgenic mouse model that over-expression of IDO in the lungs might cause an anti-asthmatic effect by diminishing proliferation, numbers and cytokine production of CD4 + T cells . Others have also previously shown that after in vivo aeroallergen exposure, serum IDO activity was increased in asymptomatic atopics compared with either symptomatic atopic or non-atopic individuals . When exposing in vitro monocyte-derived dendritic cells with house dust mite Dermatophagoides pteronyssinus 1, functionally active IDO decreased in cells from patients with house dust mite-sensitive asthma compared to non-atopic asthmatics . In asthmatic patients, the baseline IDO activity in sputum has been shown to be significantly lower than control levels, but normal baseline activity in asthmatic patients could be induced by using inhaled corticosteroids . We have previously demonstrated that a high expression of epithelial and leukocyte IDO is associated with chronic rhinosinusitis with nasal polyps, while the expression in chronic rhinosinusitis without nasal polyps remained at the control level . Thus in the upper airways, in contrast to lower airways, it seems that IDO might have a role in the nasal polyp pathomechanisms instead of atopy. Yet, more studies are required to bring evidence on this.
The expression of IDO differs between tissues . Recently, two isoforms of IDO have been studied, IDO1 and IDO2. The expression and activity of both isoform differs in different tissues and in same cell cultures . Both isoforms therefore might differ somehow in their roles [26, 27]. Having this in mind, it could be possible that the anti-IDO mAb we used could be specific only for the IDO1 isotope . Also, in some tissues IDO expression does not correlate with its activity. Indeed, elevated expression of IDO can translate into little activity or no activity at all . Even though high levels of IDO expression can be measured, this does not necessarily translate into activity measured by ratio of tryptophan over kynurenine.
Both atopic asthma and atopic rhinitis are complex diseases with different phenotypes and genetic backgrounds. Currently it is thought that patients with certain (epi)genetic elements are prone to have immunological dysfunctions of respiratory barriers putatively by stimulation by certain environmental interactions . Thus, our findings suggest that adult patients with only birch pollen AR but not asthma symptoms do not have local IDO. In the future, it would be of interest to observe whether immunological factors differ in patients having only the AR phenotype compared to those with the AR and asthma phenotype .