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A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue

Exposure to environmental stressors such as cigarette smoke (CS) elicits a variety of biological responses in humans, including the induction of inflammatory responses. These responses are especially pronounced in the lung, where pulmonary cells sit at the interface between the body’s internal and e...

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Autores principales: Westra, Jurjen W., Schlage, Walter K., Hengstermann, Arnd, Gebel, Stephan, Mathis, Carole, Thomson, Ty, Wong, Ben, Hoang, Vy, Veljkovic, Emilija, Peck, Michael, Lichtner, Rosemarie B., Weisensee, Dirk, Talikka, Marja, Deehan, Renee, Hoeng, Julia, Peitsch, Manuel C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Libertas Academica 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700945/
https://www.ncbi.nlm.nih.gov/pubmed/23843693
http://dx.doi.org/10.4137/BBI.S11509
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author Westra, Jurjen W.
Schlage, Walter K.
Hengstermann, Arnd
Gebel, Stephan
Mathis, Carole
Thomson, Ty
Wong, Ben
Hoang, Vy
Veljkovic, Emilija
Peck, Michael
Lichtner, Rosemarie B.
Weisensee, Dirk
Talikka, Marja
Deehan, Renee
Hoeng, Julia
Peitsch, Manuel C.
author_facet Westra, Jurjen W.
Schlage, Walter K.
Hengstermann, Arnd
Gebel, Stephan
Mathis, Carole
Thomson, Ty
Wong, Ben
Hoang, Vy
Veljkovic, Emilija
Peck, Michael
Lichtner, Rosemarie B.
Weisensee, Dirk
Talikka, Marja
Deehan, Renee
Hoeng, Julia
Peitsch, Manuel C.
author_sort Westra, Jurjen W.
collection PubMed
description Exposure to environmental stressors such as cigarette smoke (CS) elicits a variety of biological responses in humans, including the induction of inflammatory responses. These responses are especially pronounced in the lung, where pulmonary cells sit at the interface between the body’s internal and external environments. We combined a literature survey with a computational analysis of multiple transcriptomic data sets to construct a computable causal network model (the Inflammatory Process Network (IPN)) of the main pulmonary inflammatory processes. The IPN model predicted decreased epithelial cell barrier defenses and increased mucus hypersecretion in human bronchial epithelial cells, and an attenuated pro-inflammatory (M1) profile in alveolar macrophages following exposure to CS, consistent with prior results. The IPN provides a comprehensive framework of experimentally supported pathways related to CS-induced pulmonary inflammation. The IPN is freely available to the scientific community as a resource with broad applicability to study the pathogenesis of pulmonary disease.
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spelling pubmed-37009452013-07-10 A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue Westra, Jurjen W. Schlage, Walter K. Hengstermann, Arnd Gebel, Stephan Mathis, Carole Thomson, Ty Wong, Ben Hoang, Vy Veljkovic, Emilija Peck, Michael Lichtner, Rosemarie B. Weisensee, Dirk Talikka, Marja Deehan, Renee Hoeng, Julia Peitsch, Manuel C. Bioinform Biol Insights Original Research Exposure to environmental stressors such as cigarette smoke (CS) elicits a variety of biological responses in humans, including the induction of inflammatory responses. These responses are especially pronounced in the lung, where pulmonary cells sit at the interface between the body’s internal and external environments. We combined a literature survey with a computational analysis of multiple transcriptomic data sets to construct a computable causal network model (the Inflammatory Process Network (IPN)) of the main pulmonary inflammatory processes. The IPN model predicted decreased epithelial cell barrier defenses and increased mucus hypersecretion in human bronchial epithelial cells, and an attenuated pro-inflammatory (M1) profile in alveolar macrophages following exposure to CS, consistent with prior results. The IPN provides a comprehensive framework of experimentally supported pathways related to CS-induced pulmonary inflammation. The IPN is freely available to the scientific community as a resource with broad applicability to study the pathogenesis of pulmonary disease. Libertas Academica 2013-06-20 /pmc/articles/PMC3700945/ /pubmed/23843693 http://dx.doi.org/10.4137/BBI.S11509 Text en © 2013 the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article published under the Creative Commons CC-BY-NC 3.0 license.
spellingShingle Original Research
Westra, Jurjen W.
Schlage, Walter K.
Hengstermann, Arnd
Gebel, Stephan
Mathis, Carole
Thomson, Ty
Wong, Ben
Hoang, Vy
Veljkovic, Emilija
Peck, Michael
Lichtner, Rosemarie B.
Weisensee, Dirk
Talikka, Marja
Deehan, Renee
Hoeng, Julia
Peitsch, Manuel C.
A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title_full A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title_fullStr A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title_full_unstemmed A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title_short A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue
title_sort modular cell-type focused inflammatory process network model for non-diseased pulmonary tissue
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700945/
https://www.ncbi.nlm.nih.gov/pubmed/23843693
http://dx.doi.org/10.4137/BBI.S11509
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