Publication

Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma

Osei, E. T., B Mostaço-Guidolin, L., Hsieh, A., Warner, S. M., Al-Fouadi, M., Wang, M., Cole, D. J., Maksym, G. N., S Hallstrand, T., Timens, W., Brandsma, C-A., Heijink, I. H. & Hackett, T-L., 26-May-2020, In : Scientific Reports. 10, 1, 14 p., 8721.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Osei, E. T., B Mostaço-Guidolin, L., Hsieh, A., Warner, S. M., Al-Fouadi, M., Wang, M., Cole, D. J., Maksym, G. N., S Hallstrand, T., Timens, W., Brandsma, C-A., Heijink, I. H., & Hackett, T-L. (2020). Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma. Scientific Reports, 10(1), [8721]. https://doi.org/10.1038/s41598-020-65567-z

Author

Osei, Emmanuel T ; B Mostaço-Guidolin, Leila ; Hsieh, Aileen ; Warner, Stephanie M ; Al-Fouadi, May ; Wang, Mary ; Cole, Darren J ; Maksym, Geoffrey N ; S Hallstrand, Teal ; Timens, Wim ; Brandsma, Corry-Anke ; Heijink, Irene H ; Hackett, Tillie-Louise. / Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts : Implications for asthma. In: Scientific Reports. 2020 ; Vol. 10, No. 1.

Harvard

Osei, ET, B Mostaço-Guidolin, L, Hsieh, A, Warner, SM, Al-Fouadi, M, Wang, M, Cole, DJ, Maksym, GN, S Hallstrand, T, Timens, W, Brandsma, C-A, Heijink, IH & Hackett, T-L 2020, 'Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma', Scientific Reports, vol. 10, no. 1, 8721. https://doi.org/10.1038/s41598-020-65567-z

Standard

Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts : Implications for asthma. / Osei, Emmanuel T; B Mostaço-Guidolin, Leila; Hsieh, Aileen; Warner, Stephanie M; Al-Fouadi, May; Wang, Mary; Cole, Darren J; Maksym, Geoffrey N; S Hallstrand, Teal; Timens, Wim; Brandsma, Corry-Anke; Heijink, Irene H; Hackett, Tillie-Louise.

In: Scientific Reports, Vol. 10, No. 1, 8721, 26.05.2020.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Osei ET, B Mostaço-Guidolin L, Hsieh A, Warner SM, Al-Fouadi M, Wang M et al. Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma. Scientific Reports. 2020 May 26;10(1). 8721. https://doi.org/10.1038/s41598-020-65567-z


BibTeX

@article{cf3098c99aa4491e958484efa035f37a,
title = "Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts: Implications for asthma",
abstract = "In asthma, the airway epithelium has an impaired capacity to differentiate and plays a key role in the development of airway inflammation and remodeling through mediator release. The study objective was to investigate the release of (IL)-1 family members from primary airway epithelial-cells during differentiation, and how they affect primary airway fibroblast (PAF)-induced inflammation, extracellular matrix (ECM) production, and collagen I remodeling. The release of IL-1α/β and IL-33 during airway epithelial differentiation was assessed over 20-days using air-liquid interface cultures. The effect of IL-1 family cytokines on airway fibroblasts grown on collagen-coated well-plates and 3-dimensional collagen gels was assessed by measurement of inflammatory mediators and ECM proteins by ELISA and western blot, as well as collagen fiber formation using non-linear optical microscopy after 24-hours. The production of IL-1α is elevated in undifferentiated asthmatic-PAECs compared to controls. IL-1α/β induced fibroblast pro-inflammatory responses (CXCL8/IL-8, IL-6, TSLP, GM-CSF) and suppressed ECM-production (collagen, fibronectin, periostin) and the cell's ability to repair and remodel fibrillar collagen I via LOX, LOXL1 and LOXL2 activity, as confirmed by inhibition with β-aminopropionitrile. These data support a role for epithelial-derived-IL-1 in the dysregulated repair of the asthmatic-EMTU and provides new insights into the contribution of airway fibroblasts in inflammation and airway remodeling in asthma.",
author = "Osei, {Emmanuel T} and {B Mosta{\c c}o-Guidolin}, Leila and Aileen Hsieh and Warner, {Stephanie M} and May Al-Fouadi and Mary Wang and Cole, {Darren J} and Maksym, {Geoffrey N} and {S Hallstrand}, Teal and Wim Timens and Corry-Anke Brandsma and Heijink, {Irene H} and Tillie-Louise Hackett",
year = "2020",
month = may,
day = "26",
doi = "10.1038/s41598-020-65567-z",
language = "English",
volume = "10",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - Epithelial-interleukin-1 inhibits collagen formation by airway fibroblasts

T2 - Implications for asthma

AU - Osei, Emmanuel T

AU - B Mostaço-Guidolin, Leila

AU - Hsieh, Aileen

AU - Warner, Stephanie M

AU - Al-Fouadi, May

AU - Wang, Mary

AU - Cole, Darren J

AU - Maksym, Geoffrey N

AU - S Hallstrand, Teal

AU - Timens, Wim

AU - Brandsma, Corry-Anke

AU - Heijink, Irene H

AU - Hackett, Tillie-Louise

PY - 2020/5/26

Y1 - 2020/5/26

N2 - In asthma, the airway epithelium has an impaired capacity to differentiate and plays a key role in the development of airway inflammation and remodeling through mediator release. The study objective was to investigate the release of (IL)-1 family members from primary airway epithelial-cells during differentiation, and how they affect primary airway fibroblast (PAF)-induced inflammation, extracellular matrix (ECM) production, and collagen I remodeling. The release of IL-1α/β and IL-33 during airway epithelial differentiation was assessed over 20-days using air-liquid interface cultures. The effect of IL-1 family cytokines on airway fibroblasts grown on collagen-coated well-plates and 3-dimensional collagen gels was assessed by measurement of inflammatory mediators and ECM proteins by ELISA and western blot, as well as collagen fiber formation using non-linear optical microscopy after 24-hours. The production of IL-1α is elevated in undifferentiated asthmatic-PAECs compared to controls. IL-1α/β induced fibroblast pro-inflammatory responses (CXCL8/IL-8, IL-6, TSLP, GM-CSF) and suppressed ECM-production (collagen, fibronectin, periostin) and the cell's ability to repair and remodel fibrillar collagen I via LOX, LOXL1 and LOXL2 activity, as confirmed by inhibition with β-aminopropionitrile. These data support a role for epithelial-derived-IL-1 in the dysregulated repair of the asthmatic-EMTU and provides new insights into the contribution of airway fibroblasts in inflammation and airway remodeling in asthma.

AB - In asthma, the airway epithelium has an impaired capacity to differentiate and plays a key role in the development of airway inflammation and remodeling through mediator release. The study objective was to investigate the release of (IL)-1 family members from primary airway epithelial-cells during differentiation, and how they affect primary airway fibroblast (PAF)-induced inflammation, extracellular matrix (ECM) production, and collagen I remodeling. The release of IL-1α/β and IL-33 during airway epithelial differentiation was assessed over 20-days using air-liquid interface cultures. The effect of IL-1 family cytokines on airway fibroblasts grown on collagen-coated well-plates and 3-dimensional collagen gels was assessed by measurement of inflammatory mediators and ECM proteins by ELISA and western blot, as well as collagen fiber formation using non-linear optical microscopy after 24-hours. The production of IL-1α is elevated in undifferentiated asthmatic-PAECs compared to controls. IL-1α/β induced fibroblast pro-inflammatory responses (CXCL8/IL-8, IL-6, TSLP, GM-CSF) and suppressed ECM-production (collagen, fibronectin, periostin) and the cell's ability to repair and remodel fibrillar collagen I via LOX, LOXL1 and LOXL2 activity, as confirmed by inhibition with β-aminopropionitrile. These data support a role for epithelial-derived-IL-1 in the dysregulated repair of the asthmatic-EMTU and provides new insights into the contribution of airway fibroblasts in inflammation and airway remodeling in asthma.

U2 - 10.1038/s41598-020-65567-z

DO - 10.1038/s41598-020-65567-z

M3 - Article

C2 - 32457454

VL - 10

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 8721

ER -

ID: 126101344