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.