ArticleBiomaterials science2022
Destructive fibrotic teamwork: how both microenvironment stiffness and profibrotic interleukin 13 impair alveolar macrophage phenotype and function.
Article in Biomaterials science, 2022. 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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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- High-throughput bioprinted 3D cultures for probing host-pathogen interactions in bioinspired microenvironments.RSC applied polymers · 2026Article
- Effects and potential mechanisms of the ultra-high dose rate radiotherapy on lung injury: a review.Radiation oncology (London, England) · 2025Review
- Mechanical cues orchestrate monocyte behavior in immune regulation and disease.APL bioengineering · 2025Review
- Nanoparticle-Based Pulmonary Immune Engineering.Annual review of chemical and biomolecular engineering · 2025Review
- M2 macrophage co-culture overrides viscoelastic hydrogel mechanics to promote IL6-dependent fibroblast activation.Cell biomaterials · 2025Article
- Macrophage variance: investigating how macrophage origin influences responses to soluble and physical cues with immortalized vs. primary cells in 2D and 3D culture.Frontiers in biomaterials science · 2024Article
- On the path to predicting immune responses in the lung: Modeling the pulmonary innate immune system at the air-liquid interface (ALI).European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2023Review
- Interleukin-13 (IL-13)-A Pleiotropic Cytokine Involved in Wound Healing and Fibrosis.International journal of molecular sciences · 2023Review
- Aerosol pulmonary immune engineering.Advanced drug delivery reviews · 2023Review
- Systematic d-Amino Acid Substitutions to Control Peptide and Hydrogel Degradation in Cellular Microenvironments.ACS macro letters · 2023Article
- Nebulization of Model Hydrogel Nanoparticles to Macrophages at the Air-Liquid Interface.Frontiers in chemical engineering · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The pulmonary fibrotic microenvironment is characterized by increased stiffness of lung tissue and enhanced secretion of profibrotic soluble cues contributing to a feedback loop that leads to dysregulated wound healing and lung failure. Pinpointing the individual and tandem effects of profibrotic stimuli in impairing immune cell response remains difficult and is needed for improved therapeutic strategies. We utilized a statistical design of experiment (DOE) to investigate how microenvironment stiffness and interleukin 13 (IL13), a profibrotic soluble factor linked with disease severity, contribute to the impaired macrophage response commonly observed in pulmonary fibrosis. We used engineered bioinspired hydrogels of different stiffness, ranging from healthy to fibrotic lung tissue, and cultured murine alveolar macrophages (MH-S cells) with or without IL13 to quantify cell response and analyze independent and synergistic effects. We found that, while both stiffness and IL13 independently influence macrophage morphology, phenotype, phagocytosis and efferocytosis, these factors work synergistically to exacerbate impaired macrophage phenotype and efferocytosis. These unique findings provide insights into how macrophages in fibrotic conditions are not as effective in clearing debris, contributing to fibrosis initiation/progression, and more broadly inform how underlying drivers of fibrosis modulate immune cell response to facilitate therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.