Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke

Abstract The extent to which defective innate immune responses contribute to chronic obstructive pulmonary disease (COPD) is not fully understood. Pulmonary surfactant protein A (SP-A) plays an important role in regulating innate immunity in the lungs. In this study, we hypothesised that cigarette s...

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Autores principales:	Rina Takamiya, Koji Uchida, Takahiro Shibata, Toshitaka Maeno, Masaki Kato, Yoshiki Yamaguchi, Shigeru Ariki, Yoshihiro Hasegawa, Atsushi Saito, Soichi Miwa, Hiroki Takahashi, Takaaki Akaike, Yoshio Kuroki, Motoko Takahashi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1bd402c1c21d4f6cbd1e9bb410c7f097
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spelling	oai:doaj.org-article:1bd402c1c21d4f6cbd1e9bb410c7f0972021-12-02T12:30:25ZDisruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke10.1038/s41598-017-08588-52045-2322https://doaj.org/article/1bd402c1c21d4f6cbd1e9bb410c7f0972017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08588-5https://doaj.org/toc/2045-2322Abstract The extent to which defective innate immune responses contribute to chronic obstructive pulmonary disease (COPD) is not fully understood. Pulmonary surfactant protein A (SP-A) plays an important role in regulating innate immunity in the lungs. In this study, we hypothesised that cigarette smoke (CS) and its component acrolein might influence pulmonary innate immunity by affecting the function of SP-A. Indeed, acrolein-modified SP-A was detected in the lungs of mice exposed to CS for 1 week. To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry. These analyses revealed that CSE and acrolein induced hSP-A oligomerisation and that acrolein induced the modification of six residues in hSP-A: His39, His116, Cys155, Lys180, Lys221, and Cys224. These modifications had significant effects on the innate immune functions of hSP-A. CSE- or acrolein-induced modification of hSP-A significantly decreased hSP-A’s ability to inhibit bacterial growth and to enhance macrophage phagocytosis. These findings suggest that CS-induced structural and functional defects in SP-A contribute to the dysfunctional innate immune responses observed in the lung during cigarette smoking.Rina TakamiyaKoji UchidaTakahiro ShibataToshitaka MaenoMasaki KatoYoshiki YamaguchiShigeru ArikiYoshihiro HasegawaAtsushi SaitoSoichi MiwaHiroki TakahashiTakaaki AkaikeYoshio KurokiMotoko TakahashiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rina Takamiya Koji Uchida Takahiro Shibata Toshitaka Maeno Masaki Kato Yoshiki Yamaguchi Shigeru Ariki Yoshihiro Hasegawa Atsushi Saito Soichi Miwa Hiroki Takahashi Takaaki Akaike Yoshio Kuroki Motoko Takahashi Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
description	Abstract The extent to which defective innate immune responses contribute to chronic obstructive pulmonary disease (COPD) is not fully understood. Pulmonary surfactant protein A (SP-A) plays an important role in regulating innate immunity in the lungs. In this study, we hypothesised that cigarette smoke (CS) and its component acrolein might influence pulmonary innate immunity by affecting the function of SP-A. Indeed, acrolein-modified SP-A was detected in the lungs of mice exposed to CS for 1 week. To further confirm this finding, recombinant human SP-A (hSP-A) was incubated with CS extract (CSE) or acrolein and then analysed by western blotting and nanoscale liquid chromatography-matrix-assisted laser desorption/ionisation time-of-flight tandem mass spectrometry. These analyses revealed that CSE and acrolein induced hSP-A oligomerisation and that acrolein induced the modification of six residues in hSP-A: His39, His116, Cys155, Lys180, Lys221, and Cys224. These modifications had significant effects on the innate immune functions of hSP-A. CSE- or acrolein-induced modification of hSP-A significantly decreased hSP-A’s ability to inhibit bacterial growth and to enhance macrophage phagocytosis. These findings suggest that CS-induced structural and functional defects in SP-A contribute to the dysfunctional innate immune responses observed in the lung during cigarette smoking.
format	article
author	Rina Takamiya Koji Uchida Takahiro Shibata Toshitaka Maeno Masaki Kato Yoshiki Yamaguchi Shigeru Ariki Yoshihiro Hasegawa Atsushi Saito Soichi Miwa Hiroki Takahashi Takaaki Akaike Yoshio Kuroki Motoko Takahashi
author_facet	Rina Takamiya Koji Uchida Takahiro Shibata Toshitaka Maeno Masaki Kato Yoshiki Yamaguchi Shigeru Ariki Yoshihiro Hasegawa Atsushi Saito Soichi Miwa Hiroki Takahashi Takaaki Akaike Yoshio Kuroki Motoko Takahashi
author_sort	Rina Takamiya
title	Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
title_short	Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
title_full	Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
title_fullStr	Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
title_full_unstemmed	Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke
title_sort	disruption of the structural and functional features of surfactant protein a by acrolein in cigarette smoke
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/1bd402c1c21d4f6cbd1e9bb410c7f097
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Disruption of the structural and functional features of surfactant protein A by acrolein in cigarette smoke

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