ArticleCells2021
Interleukin-1α Is a Critical Mediator of the Response of Human Bronchial Fibroblasts to Eosinophilic Inflammation.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Risk factors for postoperative pulmonary complications in esophageal cancer: focus on inflammatory markers.Frontiers in oncology · 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
- Integrative Cross-Talk in Asthma: Unraveling the Complex Interactions Between Eosinophils, Immune, and Structural Cells in the Airway Microenvironment.Diagnostics (Basel, Switzerland) · 2024Review
- Biomarkers Reflecting the Severity of Bronchial Asthma in Children.Journal of asthma and allergy · 2024Article
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Understanding fibroblast-immune cell interactionsFrontiers in immunology · 2023Review
- Airway fibrin formation cascade in allergic asthma exacerbation: implications for inflammation and remodeling.Clinical proteomics · 2022Article
- An open microfluidic coculture model of fibroblasts and eosinophils to investigate mechanisms of airway inflammation.Frontiers in bioengineering and biotechnology · 2022Article
- Role of amygdala in stress-induced upregulation of airway IL-1 signaling in asthma.Biological psychology · 2022Article
- Eosinophils, beyond IL-5.Cells · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Eosinophils contribute to allergic inflammation in asthma in part via elaboration of a complex milieu of soluble mediators. Human bronchial fibroblasts (HBF) respond to stimulation by these mediators by acquiring a pro-inflammatory profile including induction of interleukin 6 (IL6) and IL8. This study sought to determine key component(s) of eosinophil soluble factors that mediate IL6 and IL8 induction in HBF. HBF treated with eosinophil-derived soluble mediators were analyzed for gene expression, intracellular signaling, and IL6 and IL8 secretion following inhibition of inflammatory signaling. Segmental allergen bronchoprovocation (SBP-Ag) was performed in mild asthmatics and bronchoalveolar lavage fluid was analyzed for eosinophils and cytokines. We found that signaling via the IL1α/IL1 receptor is an essential component of the response of HBF to eosinophil-derived soluble factors. IL1α-dependent activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) signaling is required to induce IL6 secretion. However, NFκB signaling is dispensable for the induction of IL8, whereas Src is required. IL1α is associated with eosinophilic inflammation in human airways after SBP-Ag. Conclusions: IL1α appears to be a critical component of the soluble eosinophil-derived milieu that drives pro-inflammatory bronchial fibroblast responses and associates with eosinophilic inflammation following SBP-Ag. Disruption of IL1α-signaling could modify the downstream effects of eosinophilic inflammation on airway remodeling.
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