Academic Journal
The role of type II esophageal microbiota in achalasia: Activation of macrophages and degeneration of myenteric neurons.
| Τίτλος: | The role of type II esophageal microbiota in achalasia: Activation of macrophages and degeneration of myenteric neurons. |
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| Συγγραφείς: | Geng ZH; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Zhu Y; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Chen WF; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Fu PY; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Xu JQ; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Wang TY; Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China., Yao L; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Liu ZQ; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Li XQ; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Zhang ZC; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Wang Y; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Ma LY; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Lin SL; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., He MJ; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China., Zhao C; Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China. Electronic address: czhao@fudan.edu.cn., Li QL; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China. Electronic address: li.quanlin@zs-hospital.sh.cn., Zhou PH; Endoscopy Center and Endoscopy Research Institute, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Collaborative Innovation Center of Endoscopy, Shanghai, China. Electronic address: zhou.pinghong@zs-hospital.sh.cn. |
| Πηγή: | Microbiological research [Microbiol Res] 2023 Nov; Vol. 276, pp. 127470. Date of Electronic Publication: 2023 Aug 07. |
| Τύπος έκδοσης: | Journal Article |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: G. Fischer Country of Publication: Germany NLM ID: 9437794 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1618-0623 (Electronic) Linking ISSN: 09445013 NLM ISO Abbreviation: Microbiol Res Subsets: MEDLINE |
| Imprint Name(s): | Original Publication: Jena : G. Fischer, c1994- |
| Ιατρικοί όροι (MeSH): | Esophageal Achalasia*/pathology , Gastrointestinal Microbiome*, Neurons/pathology ; Anti-Bacterial Agents/pharmacology ; Mice ; Animals ; Lipopolysaccharides ; Dysbiosis ; Mice, Inbred C57BL |
| Περίληψη: | Objective: The gut microbiota plays a critical role in the appropriate development and maintenance of the enteric nervous system (ENS). Esophageal achalasia (EA) is a rare motility disorder characterized by the selective degeneration of inhibitory neurons in the esophageal myenteric plexus. This study aimed to evaluate the composition of the esophageal microbiota in achalasia and explore the potential microbial mechanisms involved in its pathogenesis. Design: The lower esophageal mucosal microbiota was analyzed in patients with achalasia and control participants using 16 S rRNA sequencing. The association between the esophageal microbiota and achalasia was validated by inducing esophageal dysbiosis in C57BL/10 J and C57BL/10ScNJ (TLR4KO) mice via chronic exposure to ampicillin sodium in their drinking water. Results: The esophageal microbiota in EA patients had lower diversity and a predominance of Gram-negative bacteria (Type II microbiota) compared to that in the healthy controls. Additionally, the relative abundance of Rhodobacter decreased significantly in patients with achalasia, which correlated with an enrichment of lipopolysaccharide (LPS) biosynthesis based on the COG database. Antibiotic-treated mice showed an esophageal microbiota characterized by increased abundance of Gram-negative bacteria (Type II microbiome), decreased abundance of Rhodobacter, and enriched LPS biosynthesis. Compared to the control and TLR4KO mice, the antibiotic-treated wild-type mice had higher LES resting pressure, increased LES contraction rate after carbachol stimulation, and decreased relaxation response to L-arginine. Moreover, the number of myenteric neurons decreased, while the number of lamina propria macrophages (LpMs) increased after antibiotic exposure. Furthermore, the TLR4-MYD88-NF-κB pathway was up-regulated, and the production of TNF-α, IL-1β, and IL-6 increased in the antibiotic-treated mice. Conclusions: Patients with achalasia exhibit esophageal dysbiosis, which may induce aberrant esophageal motility. (Copyright © 2023 Elsevier GmbH. All rights reserved.) |
| Competing Interests: | Declaration of Competing Interest All authors have no conflicts of interest or financial ties to disclose. |
| Contributed Indexing: | Keywords: Esophageal achalasia; Esophageal microbiota; Lipopolysaccharide; Macrophage; Toll-like receptor 4 |
| Substance Nomenclature: | 0 (Lipopolysaccharides) 0 (Anti-Bacterial Agents) |
| Entry Date(s): | Date Created: 20230814 Date Completed: 20230919 Latest Revision: 20230919 |
| Update Code: | 20260130 |
| DOI: | 10.1016/j.micres.2023.127470 |
| PMID: | 37574627 |
| Βάση Δεδομένων: | MEDLINE |
| ISSN: | 1618-0623 |
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| DOI: | 10.1016/j.micres.2023.127470 |