ArticleFrontiers in bioengineering and biotechnology2022
An open microfluidic coculture model of fibroblasts and eosinophils to investigate mechanisms of airway inflammation.
Article in Frontiers in bioengineering and biotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Extracellular matrix phenotyping by imaging mass cytometry defines distinct cellular matrix environments associated with allergic airway inflammation.Molecular systems biology · 2026Article
- Injury-induced paracrine effects on the podocyte's transcriptome.American journal of physiology. Renal physiology · 2026Article
- Mast Cell Chymase and Human Lung Fibroblast Interaction: Mechanisms and Implications for Asthma.Inflammation · 2026Article
- Integrative Cross-Talk in Asthma: Unraveling the Complex Interactions Between Eosinophils, Immune, and Structural Cells in the Airway Microenvironment.Diagnostics (Basel, Switzerland) · 2024Review
- Understanding fibroblast-immune cell interactionsFrontiers in immunology · 2023Review
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Interactions between fibroblasts and immune cells play an important role in tissue inflammation. Previous studies have found that eosinophils activated with interleukin-3 (IL-3) degranulate on aggregated immunoglobulin G (IgG) and release mediators that activate fibroblasts in the lung. However, these studies were done with eosinophil-conditioned media that have the capacity to investigate only one-way signaling from eosinophils to fibroblasts. Here, we demonstrate a coculture model of primary normal human lung fibroblasts (HLFs) and human blood eosinophils from patients with allergy and asthma using an open microfluidic coculture device. In our device, the two types of cells can communicate via two-way soluble factor signaling in the shared media while being physically separated by a half wall. Initially, we assessed the level of eosinophil degranulation by their release of eosinophil-derived neurotoxin (EDN). Next, we analyzed the inflammation-associated genes and soluble factors using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and multiplex immunoassays, respectively. Our results suggest an induction of a proinflammatory fibroblast phenotype of HLFs following the coculture with degranulating eosinophils, validating our previous findings. Additionally, we present a new result that indicate potential impacts of activated HLFs back on eosinophils. This open microfluidic coculture platform provides unique opportunities to investigate the intercellular signaling between the two cell types and their roles in airway inflammation and remodeling.
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