Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice

Abstract The salivary gland is rhythmically controlled by sympathetic nerve activation from the suprachiasmatic nucleus (SCN), which functions as the main oscillator of circadian rhythms. In humans, salivary IgA concentrations reflect circadian rhythmicity, which peak during sleep. However, the mech...

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Autores principales:	Misaki Wada, Kanami Orihara, Mayo Kamagata, Koki Hama, Hiroyuki Sasaki, Atsushi Haraguchi, Hiroki Miyakawa, Atsuhito Nakao, Shigenobu Shibata
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/0f58c15365a040309315187c35317f49
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spelling	oai:doaj.org-article:0f58c15365a040309315187c35317f492021-12-02T11:52:24ZCircadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice10.1038/s41598-017-09438-02045-2322https://doaj.org/article/0f58c15365a040309315187c35317f492017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-09438-0https://doaj.org/toc/2045-2322Abstract The salivary gland is rhythmically controlled by sympathetic nerve activation from the suprachiasmatic nucleus (SCN), which functions as the main oscillator of circadian rhythms. In humans, salivary IgA concentrations reflect circadian rhythmicity, which peak during sleep. However, the mechanisms controlling this rhythmicity are not well understood. Therefore, we examined whether the timing of parasympathetic (pilocarpine) or sympathetic (norepinephrine; NE) activation affects IgA secretion in the saliva. The concentrations of saliva IgA modulated by pilocarpine activation or by a combination of pilocarpine and NE activation were the highest in the middle of the light period, independent of saliva flow rate. The circadian rhythm of IgA secretion was weakened by an SCN lesion and Clock gene mutation, suggesting the importance of the SCN and Clock gene on this rhythm. Adrenoceptor antagonists blocked both NE- and pilocarpine-induced basal secretion of IgA. Dimeric IgA binds to the polymeric immunoglobulin receptor (pIgR) on the basolateral surface of epithelial cells and forms the IgA-pIgR complex. The circadian rhythm of Pigr abundance peaked during the light period, suggesting pIgR expression upon rhythmic secretion of IgA. We speculate that activation of sympathetic nerves during sleep may protect from bacterial access to the epithelial surface through enhanced secretion of IgA.Misaki WadaKanami OriharaMayo KamagataKoki HamaHiroyuki SasakiAtsushi HaraguchiHiroki MiyakawaAtsuhito NakaoShigenobu ShibataNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Misaki Wada Kanami Orihara Mayo Kamagata Koki Hama Hiroyuki Sasaki Atsushi Haraguchi Hiroki Miyakawa Atsuhito Nakao Shigenobu Shibata Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
description	Abstract The salivary gland is rhythmically controlled by sympathetic nerve activation from the suprachiasmatic nucleus (SCN), which functions as the main oscillator of circadian rhythms. In humans, salivary IgA concentrations reflect circadian rhythmicity, which peak during sleep. However, the mechanisms controlling this rhythmicity are not well understood. Therefore, we examined whether the timing of parasympathetic (pilocarpine) or sympathetic (norepinephrine; NE) activation affects IgA secretion in the saliva. The concentrations of saliva IgA modulated by pilocarpine activation or by a combination of pilocarpine and NE activation were the highest in the middle of the light period, independent of saliva flow rate. The circadian rhythm of IgA secretion was weakened by an SCN lesion and Clock gene mutation, suggesting the importance of the SCN and Clock gene on this rhythm. Adrenoceptor antagonists blocked both NE- and pilocarpine-induced basal secretion of IgA. Dimeric IgA binds to the polymeric immunoglobulin receptor (pIgR) on the basolateral surface of epithelial cells and forms the IgA-pIgR complex. The circadian rhythm of Pigr abundance peaked during the light period, suggesting pIgR expression upon rhythmic secretion of IgA. We speculate that activation of sympathetic nerves during sleep may protect from bacterial access to the epithelial surface through enhanced secretion of IgA.
format	article
author	Misaki Wada Kanami Orihara Mayo Kamagata Koki Hama Hiroyuki Sasaki Atsushi Haraguchi Hiroki Miyakawa Atsuhito Nakao Shigenobu Shibata
author_facet	Misaki Wada Kanami Orihara Mayo Kamagata Koki Hama Hiroyuki Sasaki Atsushi Haraguchi Hiroki Miyakawa Atsuhito Nakao Shigenobu Shibata
author_sort	Misaki Wada
title	Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
title_short	Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
title_full	Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
title_fullStr	Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
title_full_unstemmed	Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice
title_sort	circadian clock-dependent increase in salivary iga secretion modulated by sympathetic receptor activation in mice
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/0f58c15365a040309315187c35317f49
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_version_	1718395030280863744

Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice

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