Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells
Recent evidence indicates that indigenous Clostridium species induce colonic regulatory T cells (Tregs), and gut lymphocytes are able to migrate to pancreatic islets in an inflammatory environment. Thus, we speculate that supplementation with the well-characterized probiotics Clostridium butyricum C...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2017-10-01
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| Series: | Frontiers in Immunology |
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| Online Access: | http://journal.frontiersin.org/article/10.3389/fimmu.2017.01345/full |
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doaj-5de48bf6a42242128ae225e331930fe7 |
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| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Lingling Jia Lingling Jia Lingling Jia Kai Shan Kai Shan Kai Shan Li-Long Pan Li-Long Pan Ninghan Feng Ninghan Feng Zhuwu Lv Yajun Sun Yajun Sun Jiahong Li Jiahong Li Chengfei Wu Chengfei Wu Hao Zhang Hao Zhang Hao Zhang Wei Chen Wei Chen Wei Chen Wei Chen Julien Diana Julien Diana Jia Sun Jia Sun Jia Sun Jia Sun Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen |
| spellingShingle |
Lingling Jia Lingling Jia Lingling Jia Kai Shan Kai Shan Kai Shan Li-Long Pan Li-Long Pan Ninghan Feng Ninghan Feng Zhuwu Lv Yajun Sun Yajun Sun Jiahong Li Jiahong Li Chengfei Wu Chengfei Wu Hao Zhang Hao Zhang Hao Zhang Wei Chen Wei Chen Wei Chen Wei Chen Julien Diana Julien Diana Jia Sun Jia Sun Jia Sun Jia Sun Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells Frontiers in Immunology type 1 diabetes butyrate-producing bacteria regulatory T cells gut microbiota regulatory T cells migration |
| author_facet |
Lingling Jia Lingling Jia Lingling Jia Kai Shan Kai Shan Kai Shan Li-Long Pan Li-Long Pan Ninghan Feng Ninghan Feng Zhuwu Lv Yajun Sun Yajun Sun Jiahong Li Jiahong Li Chengfei Wu Chengfei Wu Hao Zhang Hao Zhang Hao Zhang Wei Chen Wei Chen Wei Chen Wei Chen Julien Diana Julien Diana Jia Sun Jia Sun Jia Sun Jia Sun Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen Yong Q. Chen |
| author_sort |
Lingling Jia |
| title |
Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells |
| title_short |
Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells |
| title_full |
Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells |
| title_fullStr |
Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells |
| title_full_unstemmed |
Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T Cells |
| title_sort |
clostridium butyricum cgmcc0313.1 protects against autoimmune diabetes by modulating intestinal immune homeostasis and inducing pancreatic regulatory t cells |
| publisher |
Frontiers Media S.A. |
| series |
Frontiers in Immunology |
| issn |
1664-3224 |
| publishDate |
2017-10-01 |
| description |
Recent evidence indicates that indigenous Clostridium species induce colonic regulatory T cells (Tregs), and gut lymphocytes are able to migrate to pancreatic islets in an inflammatory environment. Thus, we speculate that supplementation with the well-characterized probiotics Clostridium butyricum CGMCC0313.1 (CB0313.1) may induce pancreatic Tregs and consequently inhibit the diabetes incidence in non-obese diabetic (NOD) mice. CB0313.1 was administered daily to female NOD mice from 3 to 45 weeks of age. The control group received an equal volume of sterile water. Fasting glucose was measured twice a week. Pyrosequencing of the gut microbiota and flow cytometry of mesenteric lymph node (MLN), pancreatic lymph node (PLN), pancreatic and splenic immune cells were performed to investigate the effect of CB0313.1 treatment. Early oral administration of CB0313.1 mitigated insulitis, delayed the onset of diabetes, and improved energy metabolic dysfunction. Protection may involve increased Tregs, rebalanced Th1/Th2/Th17 cells and changes to a less proinflammatory immunological milieu in the gut, PLN, and pancreas. An increase of α4β7+ (the gut homing receptor) Tregs in the PLN suggests that the mechanism may involve increased migration of gut-primed Tregs to the pancreas. Furthermore, 16S rRNA gene sequencing revealed that CB0313.1 enhanced the Firmicutes/Bacteroidetes ratio, enriched Clostridium-subgroups and butyrate-producing bacteria subgroups. Our results provide the basis for future clinical investigations in preventing type 1 diabetes by oral CB0313.1 administration. |
| topic |
type 1 diabetes butyrate-producing bacteria regulatory T cells gut microbiota regulatory T cells migration |
| url |
http://journal.frontiersin.org/article/10.3389/fimmu.2017.01345/full |
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1725996161765998592 |
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doaj-5de48bf6a42242128ae225e331930fe72020-11-24T21:22:22ZengFrontiers Media S.A.Frontiers in Immunology1664-32242017-10-01810.3389/fimmu.2017.01345289042Clostridium butyricum CGMCC0313.1 Protects against Autoimmune Diabetes by Modulating Intestinal Immune Homeostasis and Inducing Pancreatic Regulatory T CellsLingling Jia0Lingling Jia1Lingling Jia2Kai Shan3Kai Shan4Kai Shan5Li-Long Pan6Li-Long Pan7Ninghan Feng8Ninghan Feng9Zhuwu Lv10Yajun Sun11Yajun Sun12Jiahong Li13Jiahong Li14Chengfei Wu15Chengfei Wu16Hao Zhang17Hao Zhang18Hao Zhang19Wei Chen20Wei Chen21Wei Chen22Wei Chen23Julien Diana24Julien Diana25Jia Sun26Jia Sun27Jia Sun28Jia Sun29Yong Q. Chen30Yong Q. Chen31Yong Q. Chen32Yong Q. Chen33Yong Q. Chen34Wuxi School of Medicine, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaWuxi School of Medicine, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaWuxi School of Medicine, Jiangnan University, Wuxi, ChinaDepartment of Pharmacology, School of Pharmacy, Fudan University, Shanghai, ChinaWuxi School of Medicine, Jiangnan University, Wuxi, ChinaWuxi No. 2 Hospital, Wuxi, ChinaDepartment of Obstetrics, Nanjing Medical University Affiliated Wuxi Renmin Hospital, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaNational Engineering Research Center for Functional Food, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaNational Engineering Research Center for Functional Food, Jiangnan University, Wuxi, ChinaBeijing Innovation Centre of Food Nutrition and Human Health, Beijing Technology and Business University (BTBU), Beijing, ChinaInstitut National de la Santé et de la Recherche Médicale (INSERM), Unité 1151, Institute Necker-Enfants Malades (INEM), Centre National de la Recherche Scienctifique, Unité 8253, Paris, France0Université Paris Descartes, Sorbonne Paris Cité, Paris, FranceWuxi School of Medicine, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaNational Engineering Research Center for Functional Food, Jiangnan University, Wuxi, ChinaWuxi School of Medicine, Jiangnan University, Wuxi, ChinaState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, ChinaSchool of Food Science and Technology, Jiangnan University, Wuxi, ChinaNational Engineering Research Center for Functional Food, Jiangnan University, Wuxi, China1Department of Cancer Biology, Wake Forest School of Medicine, Winston-Salem, NC, United StatesRecent evidence indicates that indigenous Clostridium species induce colonic regulatory T cells (Tregs), and gut lymphocytes are able to migrate to pancreatic islets in an inflammatory environment. Thus, we speculate that supplementation with the well-characterized probiotics Clostridium butyricum CGMCC0313.1 (CB0313.1) may induce pancreatic Tregs and consequently inhibit the diabetes incidence in non-obese diabetic (NOD) mice. CB0313.1 was administered daily to female NOD mice from 3 to 45 weeks of age. The control group received an equal volume of sterile water. Fasting glucose was measured twice a week. Pyrosequencing of the gut microbiota and flow cytometry of mesenteric lymph node (MLN), pancreatic lymph node (PLN), pancreatic and splenic immune cells were performed to investigate the effect of CB0313.1 treatment. Early oral administration of CB0313.1 mitigated insulitis, delayed the onset of diabetes, and improved energy metabolic dysfunction. Protection may involve increased Tregs, rebalanced Th1/Th2/Th17 cells and changes to a less proinflammatory immunological milieu in the gut, PLN, and pancreas. An increase of α4β7+ (the gut homing receptor) Tregs in the PLN suggests that the mechanism may involve increased migration of gut-primed Tregs to the pancreas. Furthermore, 16S rRNA gene sequencing revealed that CB0313.1 enhanced the Firmicutes/Bacteroidetes ratio, enriched Clostridium-subgroups and butyrate-producing bacteria subgroups. Our results provide the basis for future clinical investigations in preventing type 1 diabetes by oral CB0313.1 administration.http://journal.frontiersin.org/article/10.3389/fimmu.2017.01345/fulltype 1 diabetesbutyrate-producing bacteriaregulatory T cellsgut microbiotaregulatory T cells migration |