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Responsible Editor | Enzyme's enteric nervous system is called the "second brain" of human beings.
It is composed of a very complex neural network, which not only controls the physiological functions of intestinal rhythm movement and secretion, but also participates in maintaining the stability of the mucosal immune system.
state.
However, in inflammatory bowel disease (IBD), limited by technical means, the pathological changes of the enteric nervous system and their significance have not been clarified.
Professor Liu Jie’s research group has long been committed to the study of neuroimmune regulation and new strategies for diagnosis and treatment.
In recent years, it has focused on the direct interaction between the enteric nervous system and intestinal regional immunity, trying to explore new mechanisms of inflammatory bowel disease regional immune disorders from a new perspective, and research and development Clinical intervention strategies.
On March 9, 2021, PNAS published online research results of Professor Liu Jie's research group from Huashan Hospital affiliated to Fudan University entitled "Acetylcholine ameliorates colitis by promoting IL-10 secretion of monocytic myeloid-derived suppressor cell through nAChR/ERK pathway".
This study revealed a new mechanism by which the cholinergic nervous system in the enteric nervous system regulates immune cell function through the cholinergic neurotransmitter acetylcholine (ACh), and then participates in the occurrence and development of inflammatory bowel disease.
The research team applied 3D immunofluorescence (iDISCO), high-throughput mass spectrometry, micro-RNAseq, deconvolution deep learning and other technologies, based on clinical samples and enteritis models, to establish an IBD enteric nerve-immune system interaction research system.
Studies have shown that there is significant cholinergic nerve damage in the intestines of IBD patients and mice with enteritis and a significant decrease in the content of the key neurotransmitter acetylcholine.
Enema administration of the neurotransmitter acetylcholine can significantly alleviate the symptoms and signs of enteritis in model mice, and increase the infiltration ratio of monocytic myeloid-derived suppressor cells (M-MDSCs) in the colonic lamina propria.
In the absence of MDSCs, the neurotransmitter acetylcholine (Ach) cannot induce remission of enteritis.
Further functional experiments confirmed that Ach can selectively act on M-MDSCs in the lamina propria of the colon to promote the expression of its anti-inflammatory factor IL-10, thereby enhancing its immunosuppressive function.
In-depth study of the mechanism found that the nAChR/MEK/ERK regulatory axis plays a key role in promoting the up-regulation of IL-10 expression by M-MDSCs.
This study revealed intestinal neuron damage and decreased neurotransmitter release in inflammatory bowel disease, and explained the direct regulatory effect and mechanism of the intestinal local neurotransmitter acetylcholine (Ach) on the intestinal mucosal immune system, thus suggesting the local intestine The application of acetylcholine and cholinesterase antagonists is expected to enhance the anti-inflammatory function of M-MDSCs, thereby alleviating the symptoms of inflammatory bowel disease.
The research results have important scientific significance and clinical application value for the comprehensive understanding of the pathogenesis of IBD and the development of new strategies for the treatment of IBD.
Professor Liu Jie, Associate Researcher Luo Feifei of Huashan Hospital Affiliated to Fudan University, Professor Chu Yiwei of School of Basic Medicine/Institute of Biomedicine of Fudan University as co-corresponding authors, Attending physician Zheng Wanwei, Huashan Hospital Affiliated to Fudan University, Ph.
D.
candidate Song Huan, Associate Luo Zhongguang The chief physician and Wu Hao's attending physician are the co-first authors of this article.
Original link: https:// Reprinting instructions [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights , The offender must be investigated.
It is composed of a very complex neural network, which not only controls the physiological functions of intestinal rhythm movement and secretion, but also participates in maintaining the stability of the mucosal immune system.
state.
However, in inflammatory bowel disease (IBD), limited by technical means, the pathological changes of the enteric nervous system and their significance have not been clarified.
Professor Liu Jie’s research group has long been committed to the study of neuroimmune regulation and new strategies for diagnosis and treatment.
In recent years, it has focused on the direct interaction between the enteric nervous system and intestinal regional immunity, trying to explore new mechanisms of inflammatory bowel disease regional immune disorders from a new perspective, and research and development Clinical intervention strategies.
On March 9, 2021, PNAS published online research results of Professor Liu Jie's research group from Huashan Hospital affiliated to Fudan University entitled "Acetylcholine ameliorates colitis by promoting IL-10 secretion of monocytic myeloid-derived suppressor cell through nAChR/ERK pathway".
This study revealed a new mechanism by which the cholinergic nervous system in the enteric nervous system regulates immune cell function through the cholinergic neurotransmitter acetylcholine (ACh), and then participates in the occurrence and development of inflammatory bowel disease.
The research team applied 3D immunofluorescence (iDISCO), high-throughput mass spectrometry, micro-RNAseq, deconvolution deep learning and other technologies, based on clinical samples and enteritis models, to establish an IBD enteric nerve-immune system interaction research system.
Studies have shown that there is significant cholinergic nerve damage in the intestines of IBD patients and mice with enteritis and a significant decrease in the content of the key neurotransmitter acetylcholine.
Enema administration of the neurotransmitter acetylcholine can significantly alleviate the symptoms and signs of enteritis in model mice, and increase the infiltration ratio of monocytic myeloid-derived suppressor cells (M-MDSCs) in the colonic lamina propria.
In the absence of MDSCs, the neurotransmitter acetylcholine (Ach) cannot induce remission of enteritis.
Further functional experiments confirmed that Ach can selectively act on M-MDSCs in the lamina propria of the colon to promote the expression of its anti-inflammatory factor IL-10, thereby enhancing its immunosuppressive function.
In-depth study of the mechanism found that the nAChR/MEK/ERK regulatory axis plays a key role in promoting the up-regulation of IL-10 expression by M-MDSCs.
This study revealed intestinal neuron damage and decreased neurotransmitter release in inflammatory bowel disease, and explained the direct regulatory effect and mechanism of the intestinal local neurotransmitter acetylcholine (Ach) on the intestinal mucosal immune system, thus suggesting the local intestine The application of acetylcholine and cholinesterase antagonists is expected to enhance the anti-inflammatory function of M-MDSCs, thereby alleviating the symptoms of inflammatory bowel disease.
The research results have important scientific significance and clinical application value for the comprehensive understanding of the pathogenesis of IBD and the development of new strategies for the treatment of IBD.
Professor Liu Jie, Associate Researcher Luo Feifei of Huashan Hospital Affiliated to Fudan University, Professor Chu Yiwei of School of Basic Medicine/Institute of Biomedicine of Fudan University as co-corresponding authors, Attending physician Zheng Wanwei, Huashan Hospital Affiliated to Fudan University, Ph.
D.
candidate Song Huan, Associate Luo Zhongguang The chief physician and Wu Hao's attending physician are the co-first authors of this article.
Original link: https:// Reprinting instructions [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights , The offender must be investigated.
