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DOI 10.1159/000091601

Медицинская библиотека · International archives of allergy and immunology · 2006

Lesions in the suprachiasmatic nuclei suppress inflammatory mediators in sensitized rats.

Irie Masahiro, Endo Yutaka

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND

Although bronchial asthma is well known as an inflammatory disease that shows obvious circadian rhythms of airway narrowing, it remains to be elucidated whether the suprachiasmatic nucleus (SCN), a major circadian pacemaker, regulates inflammatory mediators relevant to asthma. Thus, we investigated the effects of electrolytic lesioning of the SCN on the antigen-induced immediate allergic response and the late allergic response (LAR) in male Brown Norway rats, i.e. in a model of allergic inflammation.

METHODS

The immediate allergic response, assessed by the histamine levels in plasma and bronchoalveolar lavage fluid (BALF), and the LAR, assessed by the eosinophilic infiltration into BALF and the lamina propria mucosae of the left main bronchus, were examined in three groups of 18 rats each, including (1) an unoperated control group, (2) a sham SCN-lesioned group, and (3) an SCN-lesioned group.

RESULTS

Both the plasma histamine levels and the number of eosinophils in bronchial tissues in the SCN-lesioned group were significantly lower than those in the other groups. The concentration of histamine and the number of eosinophils in the right BALF showed a similar pattern; however, no significant differences were found. Both plasma adrenaline and noradrenaline levels were highest during the LAR, whereas the corticosterone level was lowest in the SCN-lesioned group; again, no significant differences were obtained.

CONCLUSIONS

These findings indicate that the SCN has a significant effect on the inflammatory mediators relevant to bronchial asthma.

Для цитирования: Irie Masahiro, Endo Yutaka. Lesions in the suprachiasmatic nuclei suppress inflammatory mediators in sensitized rats.. International archives of allergy and immunology. 2006. DOI: 10.1159/000091601.

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