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|a urn:nbn:de:hbz:6-15169619444
|2 urn
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|a 10.3389/fimmu.2017.01493
|2 doi
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|a eng
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|a 610 Medizin und Gesundheit
|2 23
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|a Chakraborty, Deblina
|0 http://d-nb.info/gnd/111796115X
|0 http://viaf.org/viaf/453147869470174980915
|4 aut
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|a Universitäts- und Landesbibliothek Münster
|0 http://d-nb.info/gnd/5091030-9
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|a Alarmin S100A8 Activates Alveolar Epithelial Cells in the Context of Acute Lung Injury in a TLR4-Dependent Manner
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|a [Electronic ed.]
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|c 2017-11-13
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|b Universitäts- und Landesbibliothek Münster
|c 2019-03-14
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|a 1-16
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|a Frontiers in Immunology 8 (2017) 1493, 1-16
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|a free access
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|a Alveolar epithelial cells (AECs) are an essential part of the respiratory barrier in lungs for gas exchange and protection against pathogens. Damage to AECs occurs during lung injury and PAMPs/DAMPs have been shown to activate AECs. However, their interplay as well as the mechanism of AECs’ activation especially by the alarmin S100A8/A9 is unknown. Thus, our aim was to study the mechanism of activation of AECs (type I and type II) by S100A8 and/or lipopolysaccharide (LPS) and to understand the role of endogenous S100A8/A9 in neutrophil recruitment in the lung. For our studies, we modified a previous protocol for isolation and culturing of murine AECs. Next, we stimulated the cells with S100A8 and/or LPS and analyzed cytokine/chemokine release. We also analyzed the contribution of the known S100-receptors TLR4 and RAGE in AEC activation. In a murine model of lung injury, we investigated the role of S100A8/A9 in neutrophil recruitment to lungs. S100A8 activates type I and type II cells in a dose- and time-dependent manner which could be quantified by the release of IL-6, KC, and MCP-1. We here clearly demonstrate that AEC s are activated by S100A8 via a TLR4-dependent pathway. Surprisingly, RAGE, albeit mainly expressed in lung tissue, plays no role. Additionally, we show that S100A8/A9 is an essential factor for neutrophil recruitment to lungs. We, therefore, conclude that S100A8 promotes acute lung injury via Toll-like receptor 4-dependent activation of AECs.
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|a specialized
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|a Finanziert durch den Open-Access-Publikationsfonds 2017 der Westfälischen Wilhelms-Universität Münster (WWU Münster).
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|a CC BY 4.0
|u http://creativecommons.org/licenses/by/4.0/
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|a damage-associated molecular patterns
|a S100A8
|a TLR4
|a type I alveolar epithelial cells
|a type II alveolar epithelial cells
|a IL-6
|a neutrophils
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|2 DRIVER Types
|a Artikel
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|a Text
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|a Zenker, Stefanie
|0 http://d-nb.info/gnd/1082172839
|0 http://viaf.org/viaf/76145541727896601216
|4 aut
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|a Rossaint, Jan Peter
|0 http://d-nb.info/gnd/142016365
|0 http://viaf.org/viaf/133285351
|4 aut
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|a Hölscher, Anna
|4 aut
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|a Pohlen, Michéle Yvonne
|u FB 05: Medizinische Fakultät
|0 http://d-nb.info/gnd/135602041
|4 aut
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| 700 |
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|a Zarbock, Alexander
|0 http://d-nb.info/gnd/128737107
|0 http://viaf.org/viaf/37979321
|4 aut
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| 700 |
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|a Roth, Johannes
|u FB 05: Medizinische Fakultät
|4 aut
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| 700 |
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|a Vogl, Thomas
|0 http://d-nb.info/gnd/1115013424
|0 http://viaf.org/viaf/11147543492753190493
|4 aut
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|3 Zum Volltext
|q text/html
|u https://nbn-resolving.de/urn:nbn:de:hbz:6-15169619444
|u urn:nbn:de:hbz:6-15169619444
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|3 Zum Volltext
|q application/pdf
|u https://repositorium.uni-muenster.de/document/miami/9827514a-e0ce-440e-a0b2-82059ba3f9bf/artikel_vogl_2017.pdf
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