Severe asthma developed into a major health problem since many patients suffering from this disease exhibit a high degree of resistance towards corticosteroid treatment. Thus, to date there is no effective therapy available, which frequently leads to hospitalization and necessity for critical care measurements including mechanic ventilation. While mild-to-moderate allergic asthma arises from a typical T helper 2 (TH2) cell directed allergic immune response characterized by corticosteroid-sensitive eosinophils, airway inflammation in patients suffering from severe asthma is commonly dominated by corticosteroid-insensitive neutrophils and additionally display highly proinflammatory TH17 cells. Both cell types, neutrophils and TH17 cells, bear the potential to aggravate the inflammatory response underlying formation of this disease, since they produce a plethora of mediators enabling them to communicate with structural cells of the airway wall as well as with other inflammatory cells already present in asthmatic airways. However, to date the role played by these cells in the processes leading to severe asthma is for away from being understood. This article aims to summarize the latest findings on that issue in order to give an update on the immunopathogenesis of severe asthma.
Keywords: Severe asthma, neutrophils, TH17 cells, IL-17A, ROR-γt, Body mass index, Cyclo-oxygenase 2, Chemokine (C-X-C motif) ligand, Chemokine (C-X-C motif) receptor, Epithelial neutrophil-activating protein 78.