## 1 Introduction  
Asthma is caused by chronic inflammation of the airways associated with airway wall remodeling. It is important to evaluate inflammatory status, especially in severe cases, to adapt therapeutics. Currently, the main methods to evaluate airway inflammation are sputum analysis, exhaled breath condensate, and fraction of exhaled nitric oxide (FeNO) [1].  
The receptor for advanced glycation end-products (RAGE) is a trans-membaneous receptor present in large quantities in the lungs, particularly in alveolar epithelial type I cells [2,3]. It is an important mediator in allergic airway inflammation (AAI) and asthma [4]. RAGE belongs to the immunoglobulin superfamily [5]. It is found in two major forms: membrane-bound RAGE (mRAGE) and soluble RAGE (sRAGE) [6]. Three domains compose mRAGE: an extracellular domain for the recognition and linking of RAGE ligands, a hydrophobic transmembrane domain, and an intracellular domain for activating intracellular pathways. The best-known ligands are advanced glycation end-products (AGEs), and damage-associated molecular patterns (DAMPs) also called alarmins, high mobility group box 1 protein (HMGB1), proteins from the S100 family, and beta-amyloid peptides [7]. sRAGE comprises only the extracellular domain of mRAGE. It is synthesized by alternative splicing events or proteolytic cleavage of mRAGE [6,8,9]. As a decoy receptor, it binds to mRAGE ligands without activating intracellular inflammatory signaling (Figure 1) [10].  
sRAGE seems to reflect pulmonary damage processes and has been studied as a biomarker of lung epithelial injury and alveolar fluid clearance [11]. Blood level of sRAGE is correlated with the severity and prognosis of adult and pediatric acute respiratory distress syndrome (ARDS) [12,13]. Studies show its utility for evaluating ARDS in adults and children, with elevated blood sRAGE levels. In adult ARDS, [PERSON] et al. report evidence that the initial alveolar epithelial injury with high plasma sRAGE level is an independent variable associated with 90-day mortality [14]. In pediatric ARDS, sRAGE levels were higher in a non-survivor group, associated with non-pulmonary organ failure and with mortality directly due to lung injury [15]. In this clinical context, median levels observed in these cases were strongly elevated (5000 pg/mL [2600-7200], \(p=0.005\)). Because sRAGE is more highly expressed in BAL fluid than in plasma (ratio of 4), its plasma elevation in ARDS could reflect alveolo-capillary membrane damage with marked leakage of sRAGE from BAL to plasma [16].  
Asthma being an inflammatory disease, RAGE and its soluble form might be expected to play a role in its pathogenesis. The RAGE pathway is involved and can promote allergic  
Figure 1: sRAGE synthesis and action. sRAGE is produced by alternative splicing events or by proteolytic cleavage. sRAGE includes the extracellular domain of mRAGE. On release, it acts as a decoy, trapping the mRAGE receptor ligands and blocking signal transduction.  
airway disease [4]. Mouse RAGE knockouts showed that the absence of RAGE abolished airway hypersensitivity, eosinophilic inflammation, and airway remodeling present in asthma, strong evidence that RAGE might be one of the principal mediators of asthma pathogenesis [17]. Few studies are available, and the correlation between blood sRAGE levels in young children with recurrent wheezing and its severity is still unclear [1,18]. In this study, we assessed plasma sRAGE levels in children aged 7 years and evaluated its correlation with asthma. We went on to examine the association between the environment and sRAGE levels.