Open AccessImpact of chronic rhinosinusitis on severe asthma patients
Author(s) -
TaJen Lee,
Chia Hsiang Fu,
Chun Hua Wang,
Chi Che Huang,
Chien Chia Huang,
Po Hung Chang,
Yi Wei Chen,
Chia Chen Wu,
Ching Lung Wu,
Han Pin Kuo
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0171047
Subject(s) - thymic stromal lymphopoietin , medicine , asthma , innate lymphoid cell , immunology , proinflammatory cytokine , immune system , sinusitis , nasal polyps , interleukin , interleukin 13 , inflammation , immunity , cytokine , interleukin 4
Coexistence of chronic rhinosinusitis (CRS) with asthma appears to impair asthma control. Type-2 innate lymphoid cells (ILC2s) respond to the cytokines of thymic stromal lymphopoietin (TSLP), interleukin (IL)-25 and IL-33, thus contributing to airway diseases such as CRS and asthma. We investigate whether the augmented Th 2 -cytokines in CRS might be related to sinonasal tract ILC2s corresponding to enhanced IL-25, IL-33 and TSLP release in severe asthmatics, and be involved in asthma control. Twenty-eight asthmatics (12 non-severe and 16 severe) with CRS receiving nasal surgery were enrolled. The predicted FEV 1 inversely associated with CRS severity of CT or endoscopy scores. Higher expression of Th2-driven cytokines (IL-4, IL-5, IL-9, and IL-13), TSLP, IL-25 and IL-33 in nasal tissues was observed in severe asthma. Severe asthmatics had higher ILC2 cell counts in their nasal tissues. ILC2 counts were positively correlated with Th 2 -cytokines. Nasal surgery significantly improved asthma control and lung function decline in severe asthma and CRS. The higher expression of IL-33/ILC2 axis-directed type 2 immune responses in nasal tissue of CRS brought the greater decline of lung function in severe asthma. ILC2-induced the upregulated activity of Th 2 -related cytokines in asthmatics with CRS may contribute to a recalcitrant status of asthma control.