Transcriptomic profiles of eosinophilic asthmatic patients classified according to their atopic status

<b>Background:</b> Inflammatory pathways driving eosinophilic asthma are becoming clearer over the years. Nevertheless, the entity of non-atopic asthma is still debated regarding the role of IgE in asthma pathogenesis (Pillai, P. et al. ISRN Allergy 2011). <b>Methods:</b> Asthmatic patients were recruited from the University Asthma Clinic of Liege. Threshold values used to define the eosinophilic phenotype were a sputum eosinophil count ≥ 3% or a blood eosinophil count &gt; 0.17x10⁹/L and a FE_NO ≥ 25 ppb (Coumou, H. et al. Respir Med 2018). Atopy was defined by the presence of at least one positive specific IgE (&gt;0.35 kU/L) to one or more common aeroallergens. Total RNA was extracted from 1 mL of blood and sequencing was performed using high-quality mRNA extracted from leukocytes. <b>Results:</b> Investigation of differentially expressed mRNAs comparing atopic (n=8) versus non-atopic (n=10) eosinophilic asthmatics (as defined by a FDR &lt; 0.01) demonstrated that several genes had been previously found to influence pathogenesis of asthma or allergy. Within the eosinophilic asthmatic cohort, some upregulated genes in atopic patients have been demonstrated to influence a number of key components in mecanisms related to allergic inflammation ; prostaglandin E synthase (PTGES), NADPH oxidase 1 (NOX1), prostaglandin E receptor 3 (PTGER3) or receptor activity modifying protein 1 (RAMP1). <b>Conclusions:</b> : These results provide a preliminary overview of systemic changes in atopic versus non-atopic eosinophilic asthma and identify a range of interesting genes and pathways to investigate while building a consistant and representative cohort.