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Involvement and therapeutic implications of airway epithelial barrier dysfunction in type 2 inflammation of asthma

Chinese Medical Journal 2022年第5期135卷 519-531页

作者： Xiang Dong Mei Ding Jinjin Zhang Ismail Ogülür Yagiz Pat Mübeccel Akdis Yadong Gao Cezmi A.Akdis Department of Allergology Zhongnan Hospital of Wuhan UniversityHubei Province Key Laboratory of Allergy and ImmunologyWuhanHubei 430071China Swiss Institute of Allergy and Asthma Research(SIAF) University of ZurichHerman-Burchard Strasse 9DavosSwitzerland.

Type 2 inflammation is a complex immune response and primary mechanism for several common allergic diseases including allergic rhinitis,allergic asthma,atopic dermatitis,and chronic rhinosinusitis with nasal polyps.It is the predominant type of immune response against helminths to prevent their tissue infiltration and induce their expulsion.Recent studies suggest that epithelial barrier dysfunction contributes to the development of type 2 inflammation in asthma,which may partly explain the increasing prevalence of asthma in China and around the globe.The epithelial barrier hypothesis has recently been proposed and has received great interest from the scientific community.The development of leaky epithelial barriers leads to microbial dysbiosis and the translocation of bacteria to inter-and sub-epithelial areas and the development of epithelial tissue inflammation.Accordingly,preventing the impairment and promoting the restoration of a deteriorated airway epithelial barrier represents a promising strategy for the treatment of asthma.This review introduces the interaction between type 2 inflammation and the airway epithelial barrier in asthma,the structure and molecular composition of the airway epithelial barrier,and the assessment of epithelial barrier integrity.The role of airway epithelial barrier disruption in the pathogenesis of asthma will be discussed.In addition,the possible mechanisms underlying the airway epithelial barrier dysfunction induced by allergens and environmental pollutants,and current treatments to restore the airway epithelial barrier are reviewed.

关键词： airway epithelial barrier Type 2 inflammation Asthma Allergen Environmental pollutants

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Galectin-7 overexpression destroys airway epithelial barrier in transgenic mice

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Integrative Zoology 2021年第2期16卷 270-279页

作者： Jing TIAN Ruxuan HE Yimu FAN Qianqian ZHANG Baolin TIAN Chunju ZHOU Chunyan LIU Mingjing SONG Shunying ZHAO Department of Respiratory Medicine II Beijing Children’s HospitalCapital Medical UniversityNational Center for Children’s HealthBeijingChina Virus Laboratory Beijing Children’s HospitalCapital Medical UniversityNational Center for Children’s HealthChina Key Laboratory of Human Disease Comparative Medicine National Health Commission of China(NHC)Beijing Engineering Research Center for Experimental Animal Models of Human DiseasesInstitute of Laboratory Animal SciencePeking Union Medicine CollegeChinese Academy of Medical SciencesBeijingChina

When the integrity of airway epithelium is destroyed,the ordered airway barrier no longer exists and increases sensitivity to viral infections and allergens,leading to the occurrence of airway inflammation such as asthma.Here,we found that galectin-7 transgenic(+)mice exhibited abnormal airway structures as embryos and after birth.These abnormalities included absent or substantially reduced pseudostratified columnar ciliated epithelium and increased monolayer cells with irregular arrangement and widening of intercellular spaces.Moreover,airway tissue from galectin-7 transgenic(+)mice showed evidence of impaired cell–cell junctions and decreased expression of zonula occludens-1(ZO-1)and E-cadherin.When treated with respiratory syncytial virus(RSV)or ovalbumin(OVA),galectin-7 transgenic(+)mice developed substantially increased bronchial epithelial detachment and apoptosis,airway smooth muscle and basement membrane thickening,and enhanced airway responsiveness.We found that Galectin-7 localized in the cytoplasm and nucleus of bronchial epithelial cells,and that increased apoptosis was mediated through mitochondrial release of cytochrome c and upregulated JNK1 activation and expression of caspase-3 in galectin-7 Tg(+)mice.These findings suggested that Galectin-7 causes airway structural defects and destroys airway epithelium barrier,which predispose the airways to RSV or OVA-induced epithelial apoptosis,injury,and other asthma responses.

关键词： airway epithelial barrier epithelial apoptosis galectin-7

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