Abstract
Chronic rhinosinusitis is a heterogenous and multifactorial disease, characterized by persistent inflammation of the nose and paranasal sinuses, which causes nasal obstruction, nasal discharge, facial pain, and smell disturbance. Chronic rhinosinusitis is divided into two phenotypes: chronic rhinosinusitis with nasal polyp and chronic rhinosinusitis without nasal polyp. Nasal polyps can be associated with many inflammatory cells including eosinophil cells, neutrophil cells, plasma cells, and lymphocytes. T2 endotype is characterized by the type-2 immune response and nasal polyps are associated with eosinophilic dominant infiltration. In contrast, in the T1 and T3 endotypes, chronic rhinosinusitis can be associated with neutrophilic dominant infiltration. In addition, there are mixed types of inflammation with different proportions of eosinophils-neutrophils in chronic rhinosinusitis. In the T2 endotype, there is an increase in the production of Th2 cytokines, including interleukin-4, interleukin-5, and interleukin-13, high levels of immunoglobulin-E in polyp tissue, and eosinophilia. Stimulation of Th2 cells, type-2 innate lymphoid cells, epithelial cell damage, Staphylococcus aureus enterotoxins, and autoimmune antibodies have important roles in the enhancement of Th2 cytokines and pathogenesis of chronic rhinosinusitis with nasal polyp. Monoclonal antibodies target type-2 inflammation, decrease nasal polyp size, and improve the clinical symptoms of CRSwNP patients. The present review will focus on factors involved in the pathogenesis of chronic rhinosinusitis and its treatment.