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Brain Micro-inflammation at Specific Vessels Dysregulates Organ-homeostasis Via the Activation of a New Neural Circuit
Yasunobu Arima
Takuto Ohki
Naoki Nishikawa
Kotaro Higuchi
Mitsutoshi Ota
Yuki Tanaka
Junko Nio-Kobayashi
Mohamed Elfeky
Ryota Sakai
Yuki Mori
Tadafumi Kawamoto
Andrea Stofkova
Yukihiro Sakashita
Yuji Morimoto
Masaki Kuwatani
Toshihiko Iwanaga
Yoshichika Yoshioka
Naoya Sakamoto
Akihiko Yoshimura
Mitsuyoshi Takiguchi
Saburo Sakoda
Marco Prinz
Daisuke Kamimura
Masaaki Murakami
出版
Universität
, 2017
URL
http://books.google.com.hk/books?id=a22XzgEACAAJ&hl=&source=gbs_api
註釋
Abstract: Impact of stress on diseases including gastrointestinal failure is well-known, but molecular mechanism is not understood. Here we show underlying molecular mechanism using EAE mice. Under stress conditions, EAE caused severe gastrointestinal failure with high-mortality. Mechanistically, autoreactive-pathogenic CD4+ T cells accumulated at specific vessels of boundary area of third-ventricle, thalamus, and dentate-gyrus to establish brain micro-inflammation via stress-gateway reflex. Importantly, induction of brain micro-inflammation at specific vessels by cytokine injection was sufficient to establish fatal gastrointestinal failure. Resulting micro-inflammation activated new neural pathway including neurons in paraventricular-nucleus, dorsomedial-nucleus-of-hypothalamus, and also vagal neurons to cause fatal gastrointestinal failure. Suppression of the brain micro-inflammation or blockage of these neural pathways inhibited the gastrointestinal failure. These results demonstrate direct link between brain micro-inflammation and fatal gastrointestinal disease via establishment of a new neural pathway under stress. They further suggest that brain micro-inflammation around specific vessels could be switch to activate new neural pathway(s) to regulate organ homeostasis