title: Role of Eosinophil Granulocytes in Allergic Airway Inflammation Endotypes.
abstract: Eosinophil granulocytes are intriguing members of the innate immunity system that have been considered important defenders during parasitic diseases as well as culprits during allergy-associated inflammatory diseases. Novel studies have, however, found new homoeostasis-maintaining roles for the cell. Recent clinical trials blocking different Th2 cytokines have uncovered that asthma is heterogeneous entity and forms different characteristic endotypes. Although eosinophils are present in allergic asthma with early onset, the cells may not be essential for the pathology. The cells are, however, likely disease causing in asthma with a late onset, which is often associated with chronic rhinosinusitis. Assessment of eosinophilia, fraction exhaled nitric oxide (FeNO) and periostin are markers that have emerged useful in assessing and monitoring asthma severity and endotype. Current scientific knowledge suggests that eosinophils are recruited by the inflammatory environment, activated by the innate interleukin (IL)-33 and prevented from apoptosis by both lymphocytes and innate immune cells such as type two innate immune cells. Eosinophils contain four specific granule proteins that exhibit an array of toxic and immune-modulatory activates. The granule proteins can be released by different mechanisms. Additionally, eosinophils contain a number of inflammatory cytokines and lipid mediators as well as radical oxygen species that might contribute to the disease both by the recruitment of other cells and the direct damage to supporting cells, leading to exacerbations and tissue fibrosis. This review aimed to outline current knowledge how eosinophils are recruited, activated and mediate damage to tissues and therapies used to control the cells.
authors.affiliation: Department of Medical Science, Respiratory Medicine and Allergology, Clinical Chemistry and Asthma Research Centre, Uppsala University and University Hospital, Uppsala, Sweden.|Department of Microbiology/Immunology, Faculty of Medical Sciences, School of Medicine, University of Sulaimani, Sulaimani, Iraq.
authors.forename: K
authors.initials: K
authors.lastname: Amin
authors.affiliation: Department of Medical Science, Respiratory Medicine and Allergology, Clinical Chemistry and Asthma Research Centre, Uppsala University and University Hospital, Uppsala, Sweden.
authors.forename: C
authors.initials: C
authors.lastname: Janson
authors.affiliation: Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts & the London, Queen Mary, University of London, London, UK.
authors.forename: J
authors.initials: J
authors.lastname: Bystrom
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000628:therapy; D002908:Chronic Disease; D003602:Cytotoxicity, Immunologic; D004804:Eosinophils / Q000276:immunology*; D006706:Homeostasis; D006801:Humans; D007113:Immunity, Innate; D007167:Immunotherapy; D000067596:Interleukin-33 / Q000276:immunology*; D009569:Nitric Oxide / Q000378:metabolism; D010641:Phenotype; D012220:Rhinitis / Q000276:immunology* / Q000628:therapy; D012852:Sinusitis / Q000276:immunology* / Q000628:therapy; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000067596:Interleukin-33; D009569:Nitric Oxide