ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2021
Increased IL-6 and Potential IL-6 trans-signalling in the airways after an allergen challenge.
Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 29 citations in OpenAlex.
- Bronchial Fibroblasts Respond to IL-4 Challenge With Cytokine Secretion: Role in Allergic Airway Inflammation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- Modulation of the NF-κB signaling pathway by the combined strategy of tocilizumab and dexamethasone for asthma therapy.Respiratory research · 2026Article
- Immune Training of the Interleukin 6 Gene in Airway Epithelial Cells is Central to Asthma Exacerbations.Allergy · 2026Article
- Soluble gp130 inhibits Th17 polarization in neutrophilic asthma by blocking IL-6Frontiers in immunology · 2026Article
- Identification of the Cytokines, Growth Factors and Their Receptors Expressed by Human Blood Eosinophils: A Transcriptomics Approach.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- The effects of montelukast sodium in conjunction with budesonide/formoterol on pulmonary function and serum markers (interleukin-6, tumor necrosis factor-α, eosinophils (EOS) count) in obstructive airway diseases (asthma and chronic obstructive pulmonary disease).Postepy dermatologii i alergologii · 2025Article
- Proteomic Analysis of Asthma Airway Inflammation after Allergen Challenge: A Heterogeneous Response.American journal of respiratory and critical care medicine · 2025Article
- Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Oncostatin-M Is Produced by Human Eosinophils and Expression Is Increased in Uncontrolled Severe Asthma.Allergy · 2025Article
- Integrating 16S rRNA Sequencing, Microflora Metabolism, and Network Pharmacology to Investigate the Mechanism of SBL in Alleviating HDM-Induced Allergic Rhinitis.International journal of molecular sciences · 2024Article
- Advances in non-type 2 severe asthma: from molecular insights to novel treatment strategies.The European respiratory journal · 2024Review
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Allergen provocation tests in respiratory research: building on 50 years of experience.The European respiratory journal · 2022Review
- Exploring the comorbidity mechanisms between asthma and idiopathic pulmonary fibrosis and the pharmacological mechanisms of Bu-Shen-Yi-Qi decoction therapy via network pharmacology.BMC complementary medicine and therapies · 2022Article
- Airway fibrin formation cascade in allergic asthma exacerbation: implications for inflammation and remodeling.Clinical proteomics · 2022Article
- Pharmacological OGG1 inhibition decreases murine allergic airway inflammation.Frontiers in pharmacology · 2022Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIn asthma, IL-6 is a potential cause of enhanced inflammation, tissue damage and airway dysfunction. IL-6 signalling is regulated by its receptor, which is composed of two proteins, IL-6R and GP130. In addition to their membrane form, these two proteins may be found as extracellular soluble forms. The interaction of IL-6 with soluble IL-6R (sIL-6R) can trigger IL-6 trans-signalling in cells lacking IL-6R. Conversely, the soluble form of GP130 (sGP130) competes with its membrane form to inhibit IL-6 trans-signalling.
objectivesWe aimed to analyse IL-6 trans-signalling proteins in the airways of subjects after an allergen challenge.
methodsWe used a model of segmental bronchoprovocation with an allergen (SBP-Ag) in human subjects with allergy. Before and 48 h after SBP-Ag, bronchoalveolar lavages (BALs) allowed for the analysis of proteins in BAL fluids (BALFs) by ELISA, and membrane proteins on the surface of BAL cells by flow cytometry. In addition, we performed RNA sequencing (RNA-seq) and used proteomic data to further inform on the expression of the IL-6R subunits by eosinophils, bronchial epithelial cells and lung fibroblasts. Finally, we measured the effect of IL-6 trans-signalling on bronchial fibroblasts, in vitro.
resultsIL-6, sIL-6R, sGP130 and the molar ratio of sIL-6R/sGP130 increased in the airways after SBP-Ag, suggesting the potential for enhanced IL-6 trans-signalling activity. BAL lymphocytes, monocytes and eosinophils displayed IL-6R on their surface and were all possible providers of sIL-6R, whereas GP130 was highly expressed in bronchial epithelial cells and lung fibroblasts. Finally, bronchial fibroblasts activated by IL-6 trans-signalling produced enhanced amounts of the chemokine, MCP-1 (CCL2). CONCLUSION AND CLINICAL RELEVANCE: After a bronchial allergen challenge, we found augmentation of the elements of IL-6 trans-signalling. Allergen-induced IL-6 trans-signalling activity can activate fibroblasts to produce chemokines that can further enhance inflammation and lung dysfunction.
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