Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice.
Circadian clock-dependent increase in salivary IgA secretion modulated by sympathetic receptor activation in mice.
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DOI:
10.1038/s41598-017-09438-0
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发表时间:
2017-08-18
影响因子:
4.6
通讯作者:
Shibata S
中科院分区:
文献类型:
--
作者:
Wada M;Orihara K;Kamagata M;Hama K;Sasaki H;Haraguchi A;Miyakawa H;Nakao A;Shibata S
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.
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影响因子:
4.6
作者:
Kuroda, Hiroaki;Tahara, Yu;Saito, Keisuke;Ohnishi, Nobuaki;Kubo, Yuji;Seo, Yasuhiro;Otsuka, Makiko;Fuse, Yuta;Ohura, Yuki;Hirao, Akiko;Shibata, Shigenobu
通讯作者:
Shibata, Shigenobu
影响因子:
3.1
作者:
Kozaki T;Kubokawa A;Taketomi R;Hatae K
通讯作者:
Hatae K
影响因子:
2.8
作者:
Cermakian N;Lange T;Golombek D;Sarkar D;Nakao A;Shibata S;Mazzoccoli G
通讯作者:
Mazzoccoli G
影响因子:
4.6
作者:
Sasaki H;Hattori Y;Ikeda Y;Kamagata M;Iwami S;Yasuda S;Tahara Y;Shibata S
通讯作者:
Shibata S
影响因子:
13.9
作者:
Mohawk JA;Green CB;Takahashi JS
通讯作者:
Takahashi JS