Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Eine Plattform für die Wissenschaft: Bauingenieurwesen, Architektur und Urbanistik
Epithelial growth factor receptor tyrosine kinase inhibitors alleviate house dust mite allergen Der p2‐induced IL‐6 and IL‐8
Steroid‐insensitive asthma‐related airway inflammation is associated with the expression of epidermal growth factor receptor (EGFR) tyrosine kinase in asthmatic bronchial epithelium. Proinflammatory cytokines IL‐6 and IL‐8 are related to steroid‐insensitive asthma. It is currently unknown how EGFR‐tyrosine kinase inhibitors (EGFR‐TKIs) affects house dust mite (HDM)‐induced asthma in terms of inflammatory cytokines related to steroid‐resistant asthma and further signaling pathway. Cytokine expressions and EGFR signaling pathway were performed by ELISA, reverse transcriptase PCR, real‐time PCR, and Western blot in cell‐line models. AMP‐activated protein kinase (AMPK) pathway‐related inhibitors were applied to confirm the association between EGFR‐TKI and AMPK pathway. HDM induced IL‐6 and IL‐8 in a dose‐dependent manner. Both Erlotinib (Tarceva) and Osimertinib (AZD‐9291) reduced the levels of HDM‐stimulated IL‐6 and IL‐8 levels in BEAS‐2B cells. AZD‐9291 was more effective than Erlotinib in inhibiting phospho‐EGFR, and downstream phosphatidylinositol‐3‐kinase/protein kinase B (PI3K/AKT) and phopho‐signal transducer and activator of transcription 3 (p‐STAT3) pathway signaling. In addition, AMPK pathway‐related inhibitor, Calcium‐/calmodulin‐dependent protein kinase kinase β (CaMKKβ) inhibitor, down‐regulated IL‐8, but EGFR‐TKI had no effect on AMPK pathway. Our findings highlight EGFR‐TKIs, Tarceva, and AZD‐9291, attenuate HDM‐induced inflammatory IL‐6 and IL‐8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway.
Epithelial growth factor receptor tyrosine kinase inhibitors alleviate house dust mite allergen Der p2‐induced IL‐6 and IL‐8
Steroid‐insensitive asthma‐related airway inflammation is associated with the expression of epidermal growth factor receptor (EGFR) tyrosine kinase in asthmatic bronchial epithelium. Proinflammatory cytokines IL‐6 and IL‐8 are related to steroid‐insensitive asthma. It is currently unknown how EGFR‐tyrosine kinase inhibitors (EGFR‐TKIs) affects house dust mite (HDM)‐induced asthma in terms of inflammatory cytokines related to steroid‐resistant asthma and further signaling pathway. Cytokine expressions and EGFR signaling pathway were performed by ELISA, reverse transcriptase PCR, real‐time PCR, and Western blot in cell‐line models. AMP‐activated protein kinase (AMPK) pathway‐related inhibitors were applied to confirm the association between EGFR‐TKI and AMPK pathway. HDM induced IL‐6 and IL‐8 in a dose‐dependent manner. Both Erlotinib (Tarceva) and Osimertinib (AZD‐9291) reduced the levels of HDM‐stimulated IL‐6 and IL‐8 levels in BEAS‐2B cells. AZD‐9291 was more effective than Erlotinib in inhibiting phospho‐EGFR, and downstream phosphatidylinositol‐3‐kinase/protein kinase B (PI3K/AKT) and phopho‐signal transducer and activator of transcription 3 (p‐STAT3) pathway signaling. In addition, AMPK pathway‐related inhibitor, Calcium‐/calmodulin‐dependent protein kinase kinase β (CaMKKβ) inhibitor, down‐regulated IL‐8, but EGFR‐TKI had no effect on AMPK pathway. Our findings highlight EGFR‐TKIs, Tarceva, and AZD‐9291, attenuate HDM‐induced inflammatory IL‐6 and IL‐8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway.
Epithelial growth factor receptor tyrosine kinase inhibitors alleviate house dust mite allergen Der p2‐induced IL‐6 and IL‐8
Pan, Hui‐Hsien (Autor:in) / Hsiao, Yu‐Ping (Autor:in) / Chen, Ping‐Ju (Autor:in) / Kang, Yu‐Ting (Autor:in) / Chao, Yu‐Hua (Autor:in) / Sheu, Ji‐Nan (Autor:in) / Lue, Ko‐Huang (Autor:in) / Ko, Jiunn‐Liang (Autor:in)
Environmental Toxicology ; 34 ; 476-485
01.04.2019
10 pages
Aufsatz (Zeitschrift)
Elektronische Ressource
Englisch
Seasonal Variation of House Dust Mite Allergen in Subtropical Climate
| British Library Conference Proceedings | 1994
| Wiley | 2003
| Wiley | 2003