Suppressive effects of S100A8 and S100A9 on neutrophil apoptosis by cytokine release of human bronchial epithelial cells in asthma
| Autor: | Ayoung Gu, Geunyeong Kim, Min Hwa Hong, Soo Jin Lee, Ji-Sook Lee, Eun Ju Yang, In Sik Kim, Beom Seok Park, Da Hye Kim, Ayesha Kashif |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Neutrophils
p38 mitogen-activated protein kinases medicine.medical_treatment Blotting Western Caspase 3 Apoptosis Enzyme-Linked Immunosorbent Assay Immunoglobulin E Neutrophil apoptosis S100A9 Cell Line 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine S00A9 medicine Calgranulin B Humans LY294002 Calgranulin A S100A8 Protein kinase B Cytokine biology General Medicine Asthma Caspase 9 Eosinophils Toll-Like Receptor 4 chemistry biology.protein Cancer research Cytokines 030211 gastroenterology & hepatology Research Paper |
| Zdroj: | International Journal of Medical Sciences |
| ISSN: | 1449-1907 |
| Popis: | S100A8 and S100A9 are important proteins in the pathogenesis of allergy. Asthma is an allergic lung disease, characterized by bronchial inflammation due to leukocytes, bronchoconstriction, and allergen-specific IgE. In this study, we examined the role of S100A8 and S100A9 in the interaction of cytokine release from bronchial epithelial cells, with constitutive apoptosis of neutrophils. S100A8 and S100A9 induce increased secretion of neutrophil survival cytokines such as MCP-1, IL-6 and IL-8. This secretion is suppressed by TLR4 inhibitor), LY294002, AKT inhibitor, PD98059, SB202190, SP600125, and BAY-11-7085. S100A8 and S100A9 also induce the phosphorylation of AKT, ERK, p38 MAPK and JNK, and activation of NF-κB, which were blocked after exposure to TLR4i, LY294002, AKTi, PD98059, SB202190 or SP600125. Furthermore, supernatants collected from bronchial epithelial cells after S100A8 and S100A9 stimulation suppressed the apoptosis of normal and asthmatic neutrophils. These inhibitory mechanisms are involved in suppression of caspase 9 and caspase 3 activation, and BAX expression. The degradation of MCL-1 and BCL-2 was also blocked by S100A8 and S100A9 stimulation. Essentially, neutrophil apoptosis was blocked by co-culture of normal and asthmatic neutrophils with BEAS-2B cells in the presence of S100A8 and S100A9. These findings will enable elucidation of asthma pathogenesis. |
| Databáze: | OpenAIRE |
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