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WNT-4 regulates pro-inflammatory responses driven by epithelial-mesenchymal cross-talk

Anita I.R. Spanjer, Eline M. van Dijk, Jacobien A. Noordhoek, Corry-Anke Brandsma, Wim Timens, Dirkje S. Postma, Herman Meurs, Reinoud Gosens, Irene H. Heijink
European Respiratory Journal 2016 48: PA5067; DOI: 10.1183/13993003.congress-2016.PA5067
Anita I.R. Spanjer
1Molecular Pharmacology, University of Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Eline M. van Dijk
1Molecular Pharmacology, University of Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Jacobien A. Noordhoek
2Pathology & Medical Biology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
3Pulmonology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Corry-Anke Brandsma
2Pathology & Medical Biology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Wim Timens
2Pathology & Medical Biology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Dirkje S. Postma
3Pulmonology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Herman Meurs
1Molecular Pharmacology, University of Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Reinoud Gosens
1Molecular Pharmacology, University of Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Irene H. Heijink
2Pathology & Medical Biology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
3Pulmonology, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
4Groningen Research Institute for Asthma and COPD, University of Groningen; University Medical Center Groningen, Groningen, Netherlands
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Abstract

Introduction Epithelial-fibroblast communication is a key aspect of inflammation and remodelling in COPD. We previously showed that epithelial cells drive fibroblast-induced inflammation when co-cultured. The WNT signalling pathway ligands WNT-4 and -7B are predominantly expressed in epithelial cells, while WNT-5A and -5B are mostly expressed in fibroblasts.

Aim We investigated whether WNT ligands are involved in pro-inflammatory responses that are induced in fibroblasts upon co-culture with epithelial cells.

Methods We studied inflammatory cytokine and WNT mRNA expression after co-culturing primary airway fibroblasts of COPD grade IV patients with differentiated primary airway epithelial cells of healthy donors. Functional WNT effects were investigated in MRC-5 human lung fibroblasts co-cultured with differentiated primary airway epithelial cells.

Results Co-culturing primary airway fibroblasts with differentiated airway epithelial cells did not change fibroblast WNT-5A and -5B mRNA expression, but increased epithelial WNT-4 and -7B mRNA expression. This was accompanied by increased interleukin (IL)-6 secretion, and an even stronger effect for the chemokine ligand CXCL8. Interestingly, WNT-4 stimulation reduced IL-6 and CXCL8 mRNA expression in MRC-5 fibroblasts, while WNT-7B, -5A and -5B caused an increase. Anti-WNT-4 increased IL-6, but not CXCL8 levels in a co-culture of MRC-5 fibroblasts with differentiated airway epithelial cells, whereas anti-WNT-7B, -WNT-5A and -WNT-5B had no effect.

Conclusion These data show a regulatory role for epithelial-derived WNT-4 on IL-6 production that is induced upon co-culturing epithelial cells with fibroblasts. This process may contribute to inflammation in COPD.

  • COPD - mechanism
  • Pharmacology
  • Inflammation
  • Copyright ©the authors 2016
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WNT-4 regulates pro-inflammatory responses driven by epithelial-mesenchymal cross-talk
Anita I.R. Spanjer, Eline M. van Dijk, Jacobien A. Noordhoek, Corry-Anke Brandsma, Wim Timens, Dirkje S. Postma, Herman Meurs, Reinoud Gosens, Irene H. Heijink
European Respiratory Journal Sep 2016, 48 (suppl 60) PA5067; DOI: 10.1183/13993003.congress-2016.PA5067

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WNT-4 regulates pro-inflammatory responses driven by epithelial-mesenchymal cross-talk
Anita I.R. Spanjer, Eline M. van Dijk, Jacobien A. Noordhoek, Corry-Anke Brandsma, Wim Timens, Dirkje S. Postma, Herman Meurs, Reinoud Gosens, Irene H. Heijink
European Respiratory Journal Sep 2016, 48 (suppl 60) PA5067; DOI: 10.1183/13993003.congress-2016.PA5067
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