Publication

Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells

Mertens, T. C. J., van der Does, A. M., Kistemaker, L. E., Ninaber, D. K., Taube, C. & Hiemstra, P. S., Jul-2017, In : Physiological Reports. 5, 13, 13 p., e13347.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Mertens, T. C. J., van der Does, A. M., Kistemaker, L. E., Ninaber, D. K., Taube, C., & Hiemstra, P. S. (2017). Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells. Physiological Reports, 5(13), [e13347]. https://doi.org/10.14814/phy2.13347

Author

Mertens, Tinne C J ; van der Does, Anne M ; Kistemaker, Loes E ; Ninaber, Dennis K ; Taube, Christian ; Hiemstra, Pieter S. / Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells. In: Physiological Reports. 2017 ; Vol. 5, No. 13.

Harvard

Mertens, TCJ, van der Does, AM, Kistemaker, LE, Ninaber, DK, Taube, C & Hiemstra, PS 2017, 'Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells', Physiological Reports, vol. 5, no. 13, e13347. https://doi.org/10.14814/phy2.13347

Standard

Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells. / Mertens, Tinne C J; van der Does, Anne M; Kistemaker, Loes E; Ninaber, Dennis K; Taube, Christian; Hiemstra, Pieter S.

In: Physiological Reports, Vol. 5, No. 13, e13347, 07.2017.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Mertens TCJ, van der Does AM, Kistemaker LE, Ninaber DK, Taube C, Hiemstra PS. Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells. Physiological Reports. 2017 Jul;5(13). e13347. https://doi.org/10.14814/phy2.13347


BibTeX

@article{bcd221d335414a4f90c427babb8dad40,
title = "Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells",
abstract = "Allergic airways inflammation in asthma is characterized by an airway epithelial gene signature composed of POSTN, CLCA1, and SERPINB2 This Th2 gene signature is proposed as a tool to classify patients with asthma into Th2-high and Th2-low phenotypes. However, many asthmatics smoke and the effects of cigarette smoke exposure on the epithelial Th2 gene signature are largely unknown. Therefore, we investigated the combined effect of IL-13 and whole cigarette smoke (CS) on the Th2 gene signature and the mucin-related genes MUC5AC and SPDEF in air-liquid interface differentiated human bronchial (ALI-PBEC) and tracheal epithelial cells (ALI-PTEC). Cultures were exposed to IL-13 for 14 days followed by 5 days of IL-13 with CS exposure. Alternatively, cultures were exposed once daily to CS for 14 days, followed by 5 days CS with IL-13. POSTN, SERPINB2, and CLCA1 expression were measured 24 h after the last exposure to CS and IL-13. In both models POSTN, SERPINB2, and CLCA1 expression were increased by IL-13. CS markedly affected the IL-13-induced Th2 gene signature as indicated by a reduced POSTN, CLCA1, and MUC5AC expression in both models. In contrast, IL-13-induced SERPINB2 expression remained unaffected by CS, whereas SPDEF expression was additively increased. Importantly, cessation of CS exposure failed to restore IL-13-induced POSTN and CLCA1 expression. We show for the first time that CS differentially affects the IL-13-induced gene signature for Th2-high asthma. These findings provide novel insights into the interaction between Th2 inflammation and cigarette smoke that is important for asthma pathogenesis and biomarker-guided therapy in asthma.",
keywords = "Journal Article, BRONCHIAL EPITHELIUM, ASTHMA, interleukin 13, primary human epithelial cells, whole cigarette smoke, T helper 2, INFLAMMATION, Exposure, Mice, LEBRIKIZUMAB, HYPERPLASIA, Biomarkers, CESSATION",
author = "Mertens, {Tinne C J} and {van der Does}, {Anne M} and Kistemaker, {Loes E} and Ninaber, {Dennis K} and Christian Taube and Hiemstra, {Pieter S}",
note = "{\circledC} 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.",
year = "2017",
month = "7",
doi = "10.14814/phy2.13347",
language = "English",
volume = "5",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley",
number = "13",

}

RIS

TY - JOUR

T1 - Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells

AU - Mertens, Tinne C J

AU - van der Does, Anne M

AU - Kistemaker, Loes E

AU - Ninaber, Dennis K

AU - Taube, Christian

AU - Hiemstra, Pieter S

N1 - © 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

PY - 2017/7

Y1 - 2017/7

N2 - Allergic airways inflammation in asthma is characterized by an airway epithelial gene signature composed of POSTN, CLCA1, and SERPINB2 This Th2 gene signature is proposed as a tool to classify patients with asthma into Th2-high and Th2-low phenotypes. However, many asthmatics smoke and the effects of cigarette smoke exposure on the epithelial Th2 gene signature are largely unknown. Therefore, we investigated the combined effect of IL-13 and whole cigarette smoke (CS) on the Th2 gene signature and the mucin-related genes MUC5AC and SPDEF in air-liquid interface differentiated human bronchial (ALI-PBEC) and tracheal epithelial cells (ALI-PTEC). Cultures were exposed to IL-13 for 14 days followed by 5 days of IL-13 with CS exposure. Alternatively, cultures were exposed once daily to CS for 14 days, followed by 5 days CS with IL-13. POSTN, SERPINB2, and CLCA1 expression were measured 24 h after the last exposure to CS and IL-13. In both models POSTN, SERPINB2, and CLCA1 expression were increased by IL-13. CS markedly affected the IL-13-induced Th2 gene signature as indicated by a reduced POSTN, CLCA1, and MUC5AC expression in both models. In contrast, IL-13-induced SERPINB2 expression remained unaffected by CS, whereas SPDEF expression was additively increased. Importantly, cessation of CS exposure failed to restore IL-13-induced POSTN and CLCA1 expression. We show for the first time that CS differentially affects the IL-13-induced gene signature for Th2-high asthma. These findings provide novel insights into the interaction between Th2 inflammation and cigarette smoke that is important for asthma pathogenesis and biomarker-guided therapy in asthma.

AB - Allergic airways inflammation in asthma is characterized by an airway epithelial gene signature composed of POSTN, CLCA1, and SERPINB2 This Th2 gene signature is proposed as a tool to classify patients with asthma into Th2-high and Th2-low phenotypes. However, many asthmatics smoke and the effects of cigarette smoke exposure on the epithelial Th2 gene signature are largely unknown. Therefore, we investigated the combined effect of IL-13 and whole cigarette smoke (CS) on the Th2 gene signature and the mucin-related genes MUC5AC and SPDEF in air-liquid interface differentiated human bronchial (ALI-PBEC) and tracheal epithelial cells (ALI-PTEC). Cultures were exposed to IL-13 for 14 days followed by 5 days of IL-13 with CS exposure. Alternatively, cultures were exposed once daily to CS for 14 days, followed by 5 days CS with IL-13. POSTN, SERPINB2, and CLCA1 expression were measured 24 h after the last exposure to CS and IL-13. In both models POSTN, SERPINB2, and CLCA1 expression were increased by IL-13. CS markedly affected the IL-13-induced Th2 gene signature as indicated by a reduced POSTN, CLCA1, and MUC5AC expression in both models. In contrast, IL-13-induced SERPINB2 expression remained unaffected by CS, whereas SPDEF expression was additively increased. Importantly, cessation of CS exposure failed to restore IL-13-induced POSTN and CLCA1 expression. We show for the first time that CS differentially affects the IL-13-induced gene signature for Th2-high asthma. These findings provide novel insights into the interaction between Th2 inflammation and cigarette smoke that is important for asthma pathogenesis and biomarker-guided therapy in asthma.

KW - Journal Article

KW - BRONCHIAL EPITHELIUM

KW - ASTHMA

KW - interleukin 13

KW - primary human epithelial cells

KW - whole cigarette smoke

KW - T helper 2

KW - INFLAMMATION

KW - Exposure

KW - Mice

KW - LEBRIKIZUMAB

KW - HYPERPLASIA

KW - Biomarkers

KW - CESSATION

U2 - 10.14814/phy2.13347

DO - 10.14814/phy2.13347

M3 - Article

VL - 5

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 13

M1 - e13347

ER -

ID: 50696599