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Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis

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Harvard

Pilecki, B, Wulf-Johansson, H, Støttrup, C, Jørgensen, PT, Djiadeu, P, Nexøe, AB, Schlosser, A, Hansen, SWK, Madsen, J, Clark, HW, Nielsen, CH, Vestbo, J, Palaniyar, N, Holmskov, U & Sorensen, GL 2018, 'Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis' Frontiers in Immunology, bind 9, 3013, s. 1-12. https://doi.org/10.3389/fimmu.2018.03013

APA

Pilecki, B., Wulf-Johansson, H., Støttrup, C., Jørgensen, P. T., Djiadeu, P., Nexøe, A. B., ... Sorensen, G. L. (2018). Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis. Frontiers in Immunology, 9, 1-12. [3013]. https://doi.org/10.3389/fimmu.2018.03013

CBE

Pilecki B, Wulf-Johansson H, Støttrup C, Jørgensen PT, Djiadeu P, Nexøe AB, Schlosser A, Hansen SWK, Madsen J, Clark HW, Nielsen CH, Vestbo J, Palaniyar N, Holmskov U, Sorensen GL. 2018. Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis. Frontiers in Immunology. 9:1-12. https://doi.org/10.3389/fimmu.2018.03013

MLA

Vancouver

Author

Pilecki, Bartosz ; Wulf-Johansson, Helle ; Støttrup, Christian ; Jørgensen, Patricia Troest ; Djiadeu, Pascal ; Nexøe, Anders Bathum ; Schlosser, Anders ; Hansen, Søren Werner Karlskov ; Madsen, Jens ; Clark, Howard William ; Nielsen, Claus Henrik ; Vestbo, Jørgen ; Palaniyar, Nades ; Holmskov, Uffe ; Sorensen, Grith Lykke. / Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis. I: Frontiers in Immunology. 2018 ; Bind 9. s. 1-12.

Bibtex

@article{15d07ba720104d71a9a2d8a6e6f4dc41,
title = "Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis",
abstract = "Cigarette smoke (CS) is the main cause of chronic obstructive pulmonary disease. Surfactant protein D (SP-D) is an important anti-inflammatory protein that regulates host immune defense in the lungs. Here, we investigated the role of SP-D in a murine model of CS-induced inflammation. Pulmonary SP-D localization and abundance was compared between smoker and non-smoker individuals. For in vivo studies, wildtype, and SP-D-deficient mice were exposed to CS for either 12 weeks or 3 days. Moreover, the effect of therapeutic administration of recombinant fragment of human SP-D on the acute CS-induced changes was evaluated. Pulmonary SP-D appeared with heterogenous expression in human smokers, while mouse lung SP-D was uniformly upregulated after CS exposure. We found that SP-D-deficient mice were more susceptible to CS-induced macrophage-rich airway inflammation. SP-D deficiency influenced local pro-inflammatory cytokine levels, with increased CCL3 and interleukin-6 but decreased CXCL1. Furthermore, CS exposure caused significant upregulation of pro-inflammatory ceramides and related ceramide synthase gene transcripts in SP-D-deficient mice compared to wildtype littermates. Administration of recombinant fragment of human SP-D (rfhSP-D) alleviated CS-induced macrophage infiltration and prevented induction of ceramide synthase gene expression. Finally, rfhSP-D treatment attenuated CS-induced human epithelial cell apoptosis in vitro. Our results indicate that SP-D deficiency aggravates CS-induced lung inflammation partly through regulation of ceramide synthesis and that local SP-D enrichment rescues CS-induced inflammation.",
author = "Bartosz Pilecki and Helle Wulf-Johansson and Christian St{\o}ttrup and J{\o}rgensen, {Patricia Troest} and Pascal Djiadeu and Nex{\o}e, {Anders Bathum} and Anders Schlosser and Hansen, {S{\o}ren Werner Karlskov} and Jens Madsen and Clark, {Howard William} and Nielsen, {Claus Henrik} and J{\o}rgen Vestbo and Nades Palaniyar and Uffe Holmskov and Sorensen, {Grith Lykke}",
year = "2018",
doi = "10.3389/fimmu.2018.03013",
language = "English",
volume = "9",
pages = "1--12",
journal = "Frontiers in Immunology",
issn = "1664-3224",
publisher = "Frontiers Research Foundation",

}

RIS

TY - JOUR

T1 - Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis

AU - Pilecki, Bartosz

AU - Wulf-Johansson, Helle

AU - Støttrup, Christian

AU - Jørgensen, Patricia Troest

AU - Djiadeu, Pascal

AU - Nexøe, Anders Bathum

AU - Schlosser, Anders

AU - Hansen, Søren Werner Karlskov

AU - Madsen, Jens

AU - Clark, Howard William

AU - Nielsen, Claus Henrik

AU - Vestbo, Jørgen

AU - Palaniyar, Nades

AU - Holmskov, Uffe

AU - Sorensen, Grith Lykke

PY - 2018

Y1 - 2018

N2 - Cigarette smoke (CS) is the main cause of chronic obstructive pulmonary disease. Surfactant protein D (SP-D) is an important anti-inflammatory protein that regulates host immune defense in the lungs. Here, we investigated the role of SP-D in a murine model of CS-induced inflammation. Pulmonary SP-D localization and abundance was compared between smoker and non-smoker individuals. For in vivo studies, wildtype, and SP-D-deficient mice were exposed to CS for either 12 weeks or 3 days. Moreover, the effect of therapeutic administration of recombinant fragment of human SP-D on the acute CS-induced changes was evaluated. Pulmonary SP-D appeared with heterogenous expression in human smokers, while mouse lung SP-D was uniformly upregulated after CS exposure. We found that SP-D-deficient mice were more susceptible to CS-induced macrophage-rich airway inflammation. SP-D deficiency influenced local pro-inflammatory cytokine levels, with increased CCL3 and interleukin-6 but decreased CXCL1. Furthermore, CS exposure caused significant upregulation of pro-inflammatory ceramides and related ceramide synthase gene transcripts in SP-D-deficient mice compared to wildtype littermates. Administration of recombinant fragment of human SP-D (rfhSP-D) alleviated CS-induced macrophage infiltration and prevented induction of ceramide synthase gene expression. Finally, rfhSP-D treatment attenuated CS-induced human epithelial cell apoptosis in vitro. Our results indicate that SP-D deficiency aggravates CS-induced lung inflammation partly through regulation of ceramide synthesis and that local SP-D enrichment rescues CS-induced inflammation.

AB - Cigarette smoke (CS) is the main cause of chronic obstructive pulmonary disease. Surfactant protein D (SP-D) is an important anti-inflammatory protein that regulates host immune defense in the lungs. Here, we investigated the role of SP-D in a murine model of CS-induced inflammation. Pulmonary SP-D localization and abundance was compared between smoker and non-smoker individuals. For in vivo studies, wildtype, and SP-D-deficient mice were exposed to CS for either 12 weeks or 3 days. Moreover, the effect of therapeutic administration of recombinant fragment of human SP-D on the acute CS-induced changes was evaluated. Pulmonary SP-D appeared with heterogenous expression in human smokers, while mouse lung SP-D was uniformly upregulated after CS exposure. We found that SP-D-deficient mice were more susceptible to CS-induced macrophage-rich airway inflammation. SP-D deficiency influenced local pro-inflammatory cytokine levels, with increased CCL3 and interleukin-6 but decreased CXCL1. Furthermore, CS exposure caused significant upregulation of pro-inflammatory ceramides and related ceramide synthase gene transcripts in SP-D-deficient mice compared to wildtype littermates. Administration of recombinant fragment of human SP-D (rfhSP-D) alleviated CS-induced macrophage infiltration and prevented induction of ceramide synthase gene expression. Finally, rfhSP-D treatment attenuated CS-induced human epithelial cell apoptosis in vitro. Our results indicate that SP-D deficiency aggravates CS-induced lung inflammation partly through regulation of ceramide synthesis and that local SP-D enrichment rescues CS-induced inflammation.

U2 - 10.3389/fimmu.2018.03013

DO - 10.3389/fimmu.2018.03013

M3 - Journal article

VL - 9

SP - 1

EP - 12

JO - Frontiers in Immunology

JF - Frontiers in Immunology

SN - 1664-3224

M1 - 3013

ER -

ID: 56379658