## 4 Discussion  
This study investigated plasma sRAGE levels in asthma in children aged 7 years. The study enrolled 68 children, healthy or with asthma. The role of sRAGE in the pathogenesis of asthma in children is poorly understood. sRAGE levels have been scantly studied in children, and we currently have no reference values in the literature that are significantly different from adults. The processes of lung maturation and alveolation are thought to explain higher sRAGE levels in infants, and a decrement was observed in its levels as alveolation phenomena gradually cease [3]. In a previous study, conducted on infants aged under 1 year, we found a mean serum sRAGE level of 2203 (\(\pm\)905 SD) pg/mL in the healthy group [26]. At age 7 years, we observed a mean plasma sRAGE level of 1794 (\(\pm\)418 SD) pg/mL in healthy children. In an adult population, the mean plasma sRAGE level significantly decreased compared with 550 pg/mL in controls [27]. However, these observations need to be confirmed given the small number of studies available and the variability in the levels observed [28; 29]. Unlike ARDS, bronchial inflammation seems to be responsible for decreasing sRAGE levels in adult and pediatric health disorders. Decreased sRAGE plasma levels are associated with worsening COPD [30]. In pediatric patients, significantly lower sRAGE levels were observed in patients with asthma and a cut-off value of serum sRAGE levels for asthma diagnosis of 1080 pg/mL has been proposed. sRAGE levels could be correlated and used as a severity biomarker, with lowered levels in uncontrolled and severe asthma subgroups compared to others [18]. In these conditions, sRAGE could act as a decoy and serve as an anti-inflammatory factor to limit the activation of the RAGE cascade. If sRAGE is considered to \"block\" the inflammatory response by trapping circulating RAGE ligands, it could be \"consumed\" and so show low blood levels. Unlike the lesions induced by ARDS, asthma does not reach the alveolo-capillary membrane and so we might expect the blood levels to approach the levels found in the BAL fluid with consumption proportional to that of the inflammation of the airways. Our present study showed sRAGE levels to be  
Figure 2: sRAGE level according to tobacco exposure. sRAGE level in pg/mL. 0: no tobacco, x: tobacco. conserved in patients with asthma. This may be because almost all our patients presented controlled asthma, with normal respiratory function, and daily treatment. A well-taken inhaled corticosteroid treatment controls lung inflammation and could therefore normalize serum level of sRAGE. The study of [PERSON] et al. in clinically stable adult asthma patients demonstrated that the levels could remain relatively stable regardless of the medical therapy used [31]. In addition, the type of inflammation could modify the expected values of sRAGE. Eosinophilic or neutrophilic inflammation may influence sRAGE level [29]. In our study, eosinophil and sensitization did not impact sRAGE levels, although our asthmatic population was too small to draw any firm conclusion. Our study shows no increase in the plasma level of sRAGE in pediatric asthma. sRAGE does not appear to be a diagnostic marker for childhood asthma. However, in our study, all the children with asthma were taking inhaled corticosteroids and had normal lung function. If an effective treatment reduces bronchial inflammation, it can normalize the level of sRAGE. We therefore hypothesize that serum sRAGE assay could be a good biomarker of well-controlled asthma. It would then be useful to measure the plasma level of sRAGE in the follow-up of children with asthma: a normal level could be the indicator of controlled asthma and could help to adapt therapy. This is innovative because currently no blood biomarker is routinely used to monitor children with asthma. Environmental exposure to factors such as atmospheric pollution and tobacco smoke can cause bronchial inflammation. Decreased sRAGE levels were observed in children living in apartments.