ArticleInternational journal of medical sciences2020
Suppressive effects of S100A8 and S100A9 on neutrophil apoptosis by cytokine release of human bronchial epithelial cells in asthma.
Article in International journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 57 citations in OpenAlex.
- Targeting of MAPK-ERK1/2 signaling by metformin in asthma: an updated mechanistic insight.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Cytosolic proliferating cell nuclear antigen (PCNA) orchestrates neutrophil hyperactivation in COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Eosinophil-derived interleukin-24 compromises epithelial integrity and aggravates airway remodeling in mouse models of allergic asthma.Nature communications · 2025Article
- Targeting Calprotectin S100A8/A9 to Overcome AML Progression in DNMT3A-Mutant Cells.Current medical science · 2025Article
- Calprotectin inhibition attenuates silica-induced lung fibrosis.Inflammopharmacology · 2025Article
- Article
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- Epigenetic training of human bronchial epithelium cells by repeated rhinovirus infections.Allergy · 2024Article
- S100A8 is a prognostic signature and associated with immune response in diffuse large B-cell lymphoma.Frontiers in oncology · 2024Article
- A computational approach for the identification of key genes and biological pathways of chronic lung diseases: a systems biology approach.BMC medical genomics · 2023Article
- Asthma-associated bacterial infections: Are they protective or deleterious?The journal of allergy and clinical immunology. Global · 2023Review
- Polypropylene nanoplastic exposure leads to lung inflammation through p38-mediated NF-κB pathway due to mitochondrial damage.Particle and fibre toxicology · 2023Article
- Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis.Journal of inflammation research · 2023Review
- The immune suppressive properties of damage associated molecular patterns in the setting of sterile traumatic injury.Frontiers in immunology · 2023Review
- Basis of preventive and non-pharmacological interventions in asthma.Frontiers in public health · 2023Review
- Insights into potential mechanisms of asthma patients with COVID-19: A study based on the gene expression profiling of bronchoalveolar lavage fluid.Computers in biology and medicine · 2022Article
- Regulation of S100As Expression by Inflammatory Cytokines in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2022Article
- Effect of add-on hydroxychloroquine therapy on serum proinflammatory cytokine levels in patients with systemic lupus erythematosus.Scientific reports · 2022Article
- Sex Dimorphism of Allergen-Induced Secreted Proteins in Murine and Human Lungs.Frontiers in immunology · 2022Article
- S100A8 as a Promising Biomarker and Oncogenic Immune Protein in the Tumor Microenvironment: An Integrative Pancancer Analysis.Journal of oncology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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