Image_1_Alpha-1 antitrypsin limits neutrophil extracellular trap disruption of airway epithelial barrier function.jpg

التفاصيل البيبلوغرافية
العنوان: Image_1_Alpha-1 antitrypsin limits neutrophil extracellular trap disruption of airway epithelial barrier function.jpg
المؤلفون: K. M. Hudock (14369595), M. S. Collins (14369598), M. A. Imbrogno (14369601), E. L. Kramer (14369604), J. J. Brewington (14369607), A. Ziady (14369610), N. Zhang (4380886), J. Snowball (14369613), Y. Xu (741407), B. C. Carey (14369616), Y. Horio (14369619), S. M. O’Grady (14369622), E. J. Kopras (14369625), J. Meeker (14369628), H. Morgan (2191891), A. J. Ostmann (14369631), E. Skala (14369634), M. E. Siefert (14369637), C. L. Na (14369640), C. R. Davidson (14369643), K. Gollomp (14369646), N. Mangalmurti (14369649), B. C. Trapnell (14369652), J. P. Clancy (8863781)
سنة النشر: 2023
مصطلحات موضوعية: Immunology, Applied Immunology (incl. Antibody Engineering, Xenotransplantation and T-cell Therapies), Autoimmunity, Cellular Immunology, Humoural Immunology and Immunochemistry, Immunogenetics (incl. Genetic Immunology), Innate Immunity, Transplantation Immunology, Tumour Immunology, Immunology not elsewhere classified, Genetic Immunology, Animal Immunology, Veterinary Immunology, NETs (neutrophil extracellular traps), alpha-1 antitrypsin (A1AT), barrier function, bronchial epithelia, E-cadherin (CDH1)
الوصف: Neutrophil extracellular traps contribute to lung injury in cystic fibrosis and asthma, but the mechanisms are poorly understood. We sought to understand the impact of human NETs on barrier function in primary human bronchial epithelial and a human airway epithelial cell line. We demonstrate that NETs disrupt airway epithelial barrier function by decreasing transepithelial electrical resistance and increasing paracellular flux, partially by NET-induced airway cell apoptosis. NETs selectively impact the expression of tight junction genes claudins 4, 8 and 11. Bronchial epithelia exposed to NETs demonstrate visible gaps in E-cadherin staining, a decrease in full-length E-cadherin protein and the appearance of cleaved E-cadherin peptides. Pretreatment of NETs with alpha-1 antitrypsin (A1AT) inhibits NET serine protease activity, limits E-cadherin cleavage, decreases bronchial cell apoptosis and preserves epithelial integrity. In conclusion, NETs disrupt human airway epithelial barrier function through bronchial cell death and degradation of E-cadherin, which are limited by exogenous A1AT.
نوع الوثيقة: still image
اللغة: unknown
Relation: https://figshare.com/articles/figure/Image_1_Alpha-1_antitrypsin_limits_neutrophil_extracellular_trap_disruption_of_airway_epithelial_barrier_function_jpg/21855600
DOI: 10.3389/fimmu.2022.1023553.s001
الاتاحة: https://doi.org/10.3389/fimmu.2022.1023553.s001
Rights: CC BY 4.0
رقم الانضمام: edsbas.1093A82C
قاعدة البيانات: BASE
الوصف
DOI:10.3389/fimmu.2022.1023553.s001