ArticleJournal of innate immunity2020
Modulation of Airway Epithelial Innate Immunity and Wound Repair by M(GM-CSF) and M(M-CSF) Macrophages.
Article in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Early Life Exposure to PFOS or F‑53B is Associated with Increased Asthma Susceptibility in Offspring and Alterations in the Pulmonary Barrier, Immune Function, and Gut Microbiota.Environment & health (Washington, D.C.) · 2026Article
- Review
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Live imaging of human airway epithelial repair in precision-cut lung slices after targeted cell damage.Biochemistry and biophysics reports · 2026Article
- Lung epithelial and alveolar macrophage-like cell interactions significantly modify innate responses to bacterial endotoxin with the involvement of direct cellular contacts, TNF-α, ICAM1 and MCP-1.Frontiers in immunology · 2025Article
- Methods and Models for StudyingInternational journal of molecular sciences · 2024Review
- 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
- Breathing on chip: Dynamic flow and stretch accelerate mucociliary maturation of airway epitheliumMaterials today. Bio · 2023Article
- Review
- Article
- Dysregulated mitochondrial metabolism upon cigarette smoke exposure in various human bronchial epithelial cell models.Disease models & mechanisms · 2022Article
- The role of human mast cells in allergy and asthma.Bioengineered · 2022Review
- M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion.PloS one · 2022Article
- Modelers Modelling Models.Journal of innate immunity · 2021Article
- CD49a Identifies Polyfunctional Memory CD8 T Cell Subsets that Persist in the Lungs After Influenza Infection.Frontiers in immunology · 2021Article
- A Leak in the Dike.Journal of innate immunity · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway epithelial cells and macrophages participate in inflammatory responses to external noxious stimuli, which can cause epithelial injury. Upon injury, epithelial cells and macrophages act in concert to ensure rapid restoration of epithelial integrity. The nature of the interactions between these cell types during epithelial repair is incompletely understood. We used an in vitro human coculture model of primary bronchial epithelial cells cultured at the air-liquid interface (ALI-PBEC) and polarized primary monocyte-derived macrophages. Using this coculture, we studied the contribution of macrophages to epithelial innate immunity, wound healing capacity, and epithelial exposure to whole cigarette smoke (WCS). Coculture of ALI-PBEC with lipopolysaccharide (LPS)-activated M(GM-CSF) macrophages increased the expression of DEFB4A, CXCL8, and IL6 at 24 h in the ALI-PBEC, whereas LPS-activated M(M-CSF) macrophages only increased epithelial IL6 expression. Furthermore, wound repair was accelerated by coculture with both activated M(GM-CSF) and M(M-CSF) macrophages, also following WCS exposure. Coculture of ALI-PBEC and M(GM-CSF) macrophages resulted in increased CAMP expression in M(GM-CSF) macrophages, which was absent in M(M-CSF) macrophages. CAMP encodes LL-37, an antimicrobial peptide with immune-modulating and repair-enhancing activities. In conclusion, dynamic crosstalk between ALI-PBEC and macrophages enhances epithelial innate immunity and wound repair, even upon concomitant cigarette smoke exposure.
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