Chronic stress-induced elevation of IL-1β in the saliva and submandibular glands of mice

Psychological stress is involved in the development of various oral diseases. Alterations in the levels of cytokines in the saliva of patients with stress-related oral diseases have been reported. However, the inconsistencies in the results of these studies might be attributed to differences in the...

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Veröffentlicht in:Medical molecular morphology 2020-12, Vol.53 (4), p.238-243
Hauptverfasser: Paudel, Durga, Morikawa, Tetsuro, Yoshida, Koki, Uehara, Osamu, Giri, Sarita, Neopane, Puja, Khurelchuluun, Ariuntsetseg, Hiraki, Daichi, Sato, Jun, Abiko, Yoshihiro
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Sprache:eng
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Zusammenfassung:Psychological stress is involved in the development of various oral diseases. Alterations in the levels of cytokines in the saliva of patients with stress-related oral diseases have been reported. However, the inconsistencies in the results of these studies might be attributed to differences in the local and systemic factors in the oral cavities of the patients. We examined the effect of chronic stress on three major inflammatory cytokines Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the saliva and salivary glands of chronically stressed mice. Six-week-old C57BL/6 J mice were randomly divided into a control and a stress group. The mice in stress group were exposed to 4 h of stress daily for 10 days and subsequently saliva, as well as the submandibular glands, were collected from both groups. The expression levels of cytokines in the saliva were examined by enzyme-linked immunosorbent assay. The submandibular glands were subjected to histopathological and mRNA expression analyses. IL-1β was significantly elevated in saliva of the chronic stressed mice. Furthermore, the mRNA expression levels of both IL-1β and IL-6 were significantly elevated in the submandibular gland of chronic stressed mice. IL-1β may be a potential salivary biomarker in response to chronic stress in mice.
ISSN:1860-1480
1860-1499
DOI:10.1007/s00795-020-00250-w