Chronic rhinosinusitis in Asia

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Chronic rhinosinusitis in Asia Yuan Zhang, MD, PhD, Elien Gevaert, PhD, Hongfei Lou, MD, PhD, Xiangdong Wang, MD, PhD, Luo Zhang, MD, PhD, Claus Bachert, MD, PhD, Nan Zhang, MD, PhD Journal of Allergy and Clinical Immunology Volume 140, Issue 5, Pages 1230-1239 (November 2017) DOI: 10.1016/j.jaci.2017.09.009 Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Subepithelial eosinophils in IL-5+ polyps from Chinese patients. Paraffin slides of IL-5+ polyps from Chinese patients were stained and analyzed by using confocal microscopy. Eosinophils and EETs were stained with an anti–major basic protein (MBP; green) antibody and DNA with propidium Iodide (DNA, red), as described by Gevaert et al.68 A, The epithelium (basal membrane indicated by a solid line and epithelial cells indicated by EC) shows frequent defects in nasal polyps. Eosinophils (MBP plus cells, green) are mostly found near these defects (indicated by arrows). Scale bar = 50 μm. B, Magnification of recruited eosinophils showed that groups of eosinophils produce extracellular traps (indicated by dashed line) near the defect as a result of both cytolysis (lysed cells, dashed line) and EET formation (viable nonlysed cells, indicated by arrowhead). Scale bar = 25 μm. Journal of Allergy and Clinical Immunology 2017 140, 1230-1239DOI: (10.1016/j.jaci.2017.09.009) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 S aureus and its products can evoke release of epithelial cytokines, such as IL-33, thymic stromal lymphopoietin (TSLP), and eotaxin, which directly or indirectly can cause EET formation.70-73 In addition, S aureus and staphylococcal proteins can directly activate T cells to release IL-5, resulting in EET formation in the eosinophils.74 Direct contact between eosinophils and S aureus evokes EET formation, resulting in killing of the bacteria but also likely epithelial damage.72 As a consequence, barrier dysfunction remains or is worsened, resulting in more invasion and a cyclic enhancement of TH2 inflammation. ILC2, Type 2 Innate lymphoid cell. Journal of Allergy and Clinical Immunology 2017 140, 1230-1239DOI: (10.1016/j.jaci.2017.09.009) Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions