Abstract Rationale

Severe eosinophilic asthma is characterized by airway eosinophilia and corticosteroid-resistance, commonly overlapping with type-2 inflammation. It has been reported that CCL5 is involved in asthma exacerbation due to RNA virus infections. We hypothesized that treatment with a virus-associated ligand and a Th2-cytokine can synergistically stimulate CCL5 production in bronchial epithelial cells. We also aimed to evaluate the mechanisms underlying CCL5 production in this in vitro model and to assess the potential of JAK1 as a novel therapeutic target via the use of Ruxolitinib.