Is there a role for gut microbiota in type 1 diabetes pathogenesis?
Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to t...
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| Veröffentlicht in: | Annals of medicine (Helsinki) Jg. 49; H. 1; S. 11 - 22 |
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Taylor & Francis
02.01.2017
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| Abstract | Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported.
Key message
Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment. |
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| AbstractList | Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported. Key message Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment. Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported. Key message Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment. Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported. Key message Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment.Type 1 diabetes mellitus (T1D) is an autoimmune disease characterized by insufficient insulin production due to the destruction of insulin secreting β-cells in the Langerhans islets. A variety of factors, including chemicals, viruses, commensal bacteria and diet have been proposed to contribute to the risk of developing the disorder. In the last years, gut microbiota has been proposed as a main factor in T1D pathogenesis. Several alterations of gut microbiota composition were described both in animal model and in humans. The decrease of Firmicutes/Bacteroides ratio was the most frequent pattern described, in particular, in human studies. Furthermore, Bacteroides, Clostridium cluster XIVa, Lactobacillus, Bifidobacterium, and Prevotella relative abundances were different in healthy and affected subjects. Dysbiosis would seem to increase intestinal permeability and thus promote the development of a pro-inflammatory niche that stimulates β-cell autoimmunity in predisposed subjects. Preliminary studies on animal models were realized to investigate the role of gut microbiota modulation as therapy or prevention approach in predisposed animals: promising and stimulating results have been reported. Key message Dietary antigens and microbiota-derived products might act as triggers of T1D by causing a pro-inflammatory and metabolic dysfunctional environment. |
| Author | Delitala, Giuseppe Pes, Giovanni Mario Delitala, Alessandro P. Bibbò, Stefano Dore, Maria Pina |
| Author_xml | – sequence: 1 givenname: Stefano surname: Bibbò fullname: Bibbò, Stefano organization: Department of Clinical and Experimental Medicine, University of Sassari – sequence: 2 givenname: Maria Pina surname: Dore fullname: Dore, Maria Pina organization: Department of Clinical and Experimental Medicine, University of Sassari – sequence: 3 givenname: Giovanni Mario surname: Pes fullname: Pes, Giovanni Mario organization: Department of Clinical and Experimental Medicine, University of Sassari – sequence: 4 givenname: Giuseppe surname: Delitala fullname: Delitala, Giuseppe organization: Department of Clinical and Experimental Medicine, University of Sassari – sequence: 5 givenname: Alessandro P. surname: Delitala fullname: Delitala, Alessandro P. email: aledelitala@tiscali.it organization: Azienda Ospedaliero-Universitaria di Sassari |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27499366$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1007/s001250050869 10.1038/nrendo.2015.218 10.1136/bmj.304.6833.1020 10.1111/apm.12011 10.1038/ng.381 10.1016/S1043-4666(02)00486-6 10.2337/db13-1236 10.1152/physrev.00045.2009 10.4049/jimmunol.1001864 10.1038/nrmicro754 10.1126/science.1233521 10.1056/NEJMoa1004809 10.1001/jama.2014.5610 10.1097/01.MPG.0000159636.19346.C1 10.1038/ismej.2009.5 10.3109/07853899109148088 10.1371/journal.pone.0078687 10.3945/ajcn.110.000646 10.1128/IAI.00664-06 10.2337/db12-0526 10.1016/j.clim.2015.05.013 10.1159/000089559 10.1371/journal.pone.0025792 10.1007/s00125-005-1831-2 10.1007/s00125-014-3274-0 10.1038/nature07336 10.1186/1758-5996-6-128 10.3390/nu7115461 10.3109/08830185.2014.889130 10.1073/pnas.1108924108 10.1101/sqb.2013.78.020081 10.1053/j.gastro.2014.02.008 10.1007/s00125-006-0465-3 10.1080/0891693021000008526 10.3109/07853899708999371 10.1172/JCI60530 10.1016/j.gtc.2012.08.008 10.1038/nature13279 10.1038/ismej.2012.158 10.1053/j.gastro.2014.01.052 10.2337/dc10-2456 10.1007/s00125-009-1626-y 10.1016/j.immuni.2010.04.001 10.1111/1753-0407.12137 10.1016/S0140-6736(97)03062-6 10.1016/j.chom.2015.01.001 10.1111/j.1464-5491.1994.tb00328.x 10.1369/0022155413519650 10.1186/1475-2891-13-60 10.1016/S0140-6736(77)91258-2 10.1007/s11154-015-9309-0 10.1007/s10495-009-0339-5 10.1373/clinchem.2010.148221 10.1186/1741-7015-11-46 10.1007/s00125-012-2564-7 10.1007/BF00279136 10.2337/db14-1847 10.1371/journal.pone.0010507 10.1007/s00125-013-2941-x 10.1016/j.diabres.2008.11.010 10.1002/(SICI)1520-7560(199909/10)15:5<323::AID-DMRR53>3.0.CO;2-P 10.1017/S0954422410000247 10.2337/db12-1243 10.1126/science.1110591 10.2337/dc12-0438 10.2337/db13-1676 10.1136/gutjnl-2014-308514 10.4161/gmic.1.2.11515 10.1111/j.1462-2920.2007.01281.x 10.1080/19490976.2015.1011876 10.3109/08916939608995340 10.1016/j.coi.2013.02.006 10.1016/j.autrev.2016.02.017 10.4049/jimmunol.1201257 10.1038/nature11550 10.1155/2016/7569431 10.1038/srep03814 10.1111/ped.12243 10.1016/j.dld.2003.09.016 10.1038/ismej.2010.92 10.4049/jimmunol.1100335 10.1001/jama.290.13.1721 10.1371/journal.pone.0110440 10.1007/s00125-010-1903-9 10.3389/fmicb.2014.00678 10.1007/s00125-014-3325-6 10.1016/j.cell.2016.04.007 10.1007/s00125-002-0801-1 10.1111/j.1600-065X.2011.01075.x 10.2174/1389450115666140606111402 10.1016/j.jaut.2014.03.005 10.1111/pedi.12305 10.1073/pnas.0500178102 10.1053/j.gastro.2014.01.060 10.1038/nri3430 10.1016/j.coi.2014.07.003 10.1136/gut.2004.042481 10.1007/s00394-009-0008-z 10.4161/gmic.18604 10.2337/diacare.24.8.1460 10.1001/jama.290.13.1713 10.2337/db05-1593 10.1079/BJN19930059 10.1016/j.pharmthera.2014.12.006 10.2337/diacare.18.7.1050 10.1038/nrendo.2013.240 10.1093/ajcn/71.6.1525 10.1111/apm.12023 10.1097/QCO.0b013e3282a56a99 |
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| Keywords | type 1 diabetes mellitus probiotic autoimmunity gut permeability therapy Dysbiosis prevention |
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| References | CIT0072 CIT0071 CIT0074 CIT0073 CIT0076 CIT0075 CIT0078 CIT0111 CIT0077 CIT0110 CIT0070 CIT0113 CIT0079 CIT0112 CIT0083 Hummel S (CIT0040) 2011; 94 CIT0082 CIT0085 CIT0084 CIT0087 CIT0086 CIT0001 CIT0088 Brown CT (CIT0059) 2011; 6 CIT0081 CIT0080 Delitala AP (CIT0107) 2016 CIT0003 CIT0002 CIT0005 CIT0004 CIT0007 CIT0006 CIT0008 CIT0094 CIT0093 CIT0096 CIT0095 CIT0010 CIT0098 CIT0097 CIT0012 CIT0011 CIT0099 CIT0090 CIT0092 CIT0014 CIT0013 CIT0016 Marietta EV (CIT0042) 2013; 8 CIT0015 CIT0018 CIT0017 CIT0019 CIT0021 CIT0020 CIT0023 CIT0022 CIT0025 CIT0024 CIT0027 CIT0026 CIT0029 CIT0028 CIT0030 CIT0032 CIT0031 Elliott RB (CIT0033) 1988; 31 CIT0036 CIT0035 CIT0038 CIT0037 Meddings JB (CIT0063) 1999; 276 CIT0039 Wirth R (CIT0091) 2014; 9 CIT0041 CIT0043 CIT0045 CIT0044 Muntoni S (CIT0034) 2000; 71 Valladares R (CIT0089) 2010; 5 Viggiano D (CIT0054) 2015; 19 CIT0047 CIT0046 CIT0049 CIT0048 CIT0050 CIT0052 CIT0051 CIT0053 CIT0056 CIT0055 Bibbo S (CIT0009) 2014 CIT0058 CIT0057 CIT0061 CIT0060 CIT0062 CIT0065 CIT0064 CIT0067 CIT0100 CIT0066 CIT0109 CIT0069 CIT0102 CIT0068 CIT0101 CIT0104 CIT0103 CIT0106 CIT0105 CIT0108 |
| References_xml | – ident: CIT0030 doi: 10.1007/s001250050869 – ident: CIT0076 doi: 10.1038/nrendo.2015.218 – ident: CIT0021 doi: 10.1136/bmj.304.6833.1020 – ident: CIT0048 doi: 10.1111/apm.12011 – ident: CIT0024 doi: 10.1038/ng.381 – ident: CIT0043 doi: 10.1016/S1043-4666(02)00486-6 – ident: CIT0110 doi: 10.2337/db13-1236 – ident: CIT0005 doi: 10.1152/physrev.00045.2009 – ident: CIT0082 doi: 10.4049/jimmunol.1001864 – ident: CIT0047 doi: 10.1038/nrmicro754 – ident: CIT0111 doi: 10.1126/science.1233521 – ident: CIT0027 doi: 10.1056/NEJMoa1004809 – volume: 276 start-page: G951 year: 1999 ident: CIT0063 publication-title: Am J Physiol – ident: CIT0028 doi: 10.1001/jama.2014.5610 – ident: CIT0066 doi: 10.1097/01.MPG.0000159636.19346.C1 – start-page: 462740 year: 2014 ident: CIT0009 publication-title: J Immun Res – ident: CIT0084 doi: 10.1038/ismej.2009.5 – ident: CIT0031 doi: 10.3109/07853899109148088 – volume: 8 start-page: e78687 year: 2013 ident: CIT0042 publication-title: PLoS One doi: 10.1371/journal.pone.0078687 – volume: 94 start-page: 1821S year: 2011 ident: CIT0040 publication-title: Am J Clin Nutr doi: 10.3945/ajcn.110.000646 – ident: CIT0051 doi: 10.1128/IAI.00664-06 – ident: CIT0100 doi: 10.2337/db12-0526 – ident: CIT0074 doi: 10.1016/j.clim.2015.05.013 – ident: CIT0035 doi: 10.1159/000089559 – volume: 6 start-page: e25792 year: 2011 ident: CIT0059 publication-title: PLoS One doi: 10.1371/journal.pone.0025792 – ident: CIT0112 doi: 10.1007/s00125-005-1831-2 – ident: CIT0061 doi: 10.1007/s00125-014-3274-0 – ident: CIT0092 doi: 10.1038/nature07336 – ident: CIT0019 doi: 10.1186/1758-5996-6-128 – ident: CIT0073 doi: 10.3390/nu7115461 – ident: CIT0049 doi: 10.3109/08830185.2014.889130 – ident: CIT0088 doi: 10.1073/pnas.1108924108 – ident: CIT0006 doi: 10.1101/sqb.2013.78.020081 – ident: CIT0010 doi: 10.1053/j.gastro.2014.02.008 – ident: CIT0069 doi: 10.1007/s00125-006-0465-3 – ident: CIT0071 doi: 10.1080/0891693021000008526 – volume: 19 start-page: 1077 year: 2015 ident: CIT0054 publication-title: Europ Rev Med Pharmacol Sci – ident: CIT0022 doi: 10.3109/07853899708999371 – ident: CIT0109 doi: 10.1172/JCI60530 – ident: CIT0077 doi: 10.1016/j.gtc.2012.08.008 – ident: CIT0095 doi: 10.1038/nature13279 – ident: CIT0062 doi: 10.1038/ismej.2012.158 – ident: CIT0001 doi: 10.1053/j.gastro.2014.01.052 – ident: CIT0039 doi: 10.2337/dc10-2456 – ident: CIT0065 doi: 10.1007/s00125-009-1626-y – ident: CIT0020 doi: 10.1016/j.immuni.2010.04.001 – ident: CIT0018 doi: 10.1111/1753-0407.12137 – ident: CIT0017 doi: 10.1016/S0140-6736(97)03062-6 – ident: CIT0102 doi: 10.1016/j.chom.2015.01.001 – ident: CIT0046 doi: 10.1111/j.1464-5491.1994.tb00328.x – ident: CIT0085 doi: 10.1369/0022155413519650 – ident: CIT0056 doi: 10.1186/1475-2891-13-60 – ident: CIT0014 doi: 10.1016/S0140-6736(77)91258-2 – ident: CIT0094 doi: 10.1007/s11154-015-9309-0 – ident: CIT0093 doi: 10.1007/s10495-009-0339-5 – ident: CIT0023 doi: 10.1373/clinchem.2010.148221 – ident: CIT0098 doi: 10.1186/1741-7015-11-46 – ident: CIT0087 doi: 10.1007/s00125-012-2564-7 – volume: 31 start-page: 62 year: 1988 ident: CIT0033 publication-title: Diabetologia doi: 10.1007/BF00279136 – ident: CIT0103 doi: 10.2337/db14-1847 – volume: 5 start-page: e10507 year: 2010 ident: CIT0089 publication-title: PLoS One doi: 10.1371/journal.pone.0010507 – ident: CIT0026 doi: 10.1007/s00125-013-2941-x – ident: CIT0032 doi: 10.1016/j.diabres.2008.11.010 – ident: CIT0041 doi: 10.1002/(SICI)1520-7560(199909/10)15:5<323::AID-DMRR53>3.0.CO;2-P – ident: CIT0057 doi: 10.1017/S0954422410000247 – ident: CIT0044 doi: 10.2337/db12-1243 – ident: CIT0002 doi: 10.1126/science.1110591 – ident: CIT0025 doi: 10.2337/dc12-0438 – ident: CIT0104 doi: 10.2337/db13-1676 – ident: CIT0075 doi: 10.1136/gutjnl-2014-308514 – ident: CIT0097 doi: 10.4161/gmic.1.2.11515 – ident: CIT0058 doi: 10.1111/j.1462-2920.2007.01281.x – ident: CIT0090 doi: 10.1080/19490976.2015.1011876 – ident: CIT0029 doi: 10.3109/08916939608995340 – ident: CIT0052 doi: 10.1016/j.coi.2013.02.006 – ident: CIT0045 doi: 10.1016/j.autrev.2016.02.017 – ident: CIT0083 doi: 10.4049/jimmunol.1201257 – ident: CIT0078 doi: 10.1038/nature11550 – ident: CIT0113 doi: 10.1155/2016/7569431 – ident: CIT0060 doi: 10.1038/srep03814 – ident: CIT0105 doi: 10.1111/ped.12243 – ident: CIT0070 doi: 10.1016/j.dld.2003.09.016 – ident: CIT0099 doi: 10.1038/ismej.2010.92 – ident: CIT0053 doi: 10.4049/jimmunol.1100335 – ident: CIT0037 doi: 10.1001/jama.290.13.1721 – volume: 9 start-page: e110440 year: 2014 ident: CIT0091 publication-title: PLoS One doi: 10.1371/journal.pone.0110440 – ident: CIT0068 doi: 10.1007/s00125-010-1903-9 – ident: CIT0101 doi: 10.3389/fmicb.2014.00678 – ident: CIT0086 doi: 10.1007/s00125-014-3325-6 – ident: CIT0012 doi: 10.1016/j.cell.2016.04.007 – ident: CIT0050 doi: 10.1007/s00125-002-0801-1 – ident: CIT0080 doi: 10.1111/j.1600-065X.2011.01075.x – ident: CIT0007 doi: 10.2174/1389450115666140606111402 – ident: CIT0108 doi: 10.1016/j.jaut.2014.03.005 – ident: CIT0055 doi: 10.1111/pedi.12305 – ident: CIT0067 doi: 10.1073/pnas.0500178102 – ident: CIT0011 doi: 10.1053/j.gastro.2014.01.060 – ident: CIT0013 doi: 10.1038/nri3430 – ident: CIT0079 doi: 10.1016/j.coi.2014.07.003 – ident: CIT0064 doi: 10.1136/gut.2004.042481 – ident: CIT0036 doi: 10.1007/s00394-009-0008-z – ident: CIT0096 doi: 10.4161/gmic.18604 – ident: CIT0015 doi: 10.2337/diacare.24.8.1460 – ident: CIT0038 doi: 10.1001/jama.290.13.1713 – ident: CIT0072 doi: 10.2337/db05-1593 – ident: CIT0081 doi: 10.1079/BJN19930059 – ident: CIT0008 doi: 10.1016/j.pharmthera.2014.12.006 – ident: CIT0016 doi: 10.2337/diacare.18.7.1050 – start-page: 7347065 year: 2016 ident: CIT0107 publication-title: J Diabetes Res – ident: CIT0004 doi: 10.1038/nrendo.2013.240 – volume: 71 start-page: 1525 year: 2000 ident: CIT0034 publication-title: Am J Clin Nutr doi: 10.1093/ajcn/71.6.1525 – ident: CIT0106 doi: 10.1111/apm.12023 – ident: CIT0003 doi: 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| SubjectTerms | Animals autoimmunity Autoimmunity - physiology Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - microbiology Diabetes Mellitus, Type 1 - physiopathology Diet - adverse effects Dysbiosis Dysbiosis - immunology Gastrointestinal Microbiome - immunology gut permeability Humans Insulin-Secreting Cells - immunology Insulin-Secreting Cells - pathology Intestines - immunology Intestines - microbiology Microbiota Models, Animal Permeability prevention probiotic Probiotics - therapeutic use therapy type 1 diabetes mellitus |
| Title | Is there a role for gut microbiota in type 1 diabetes pathogenesis? |
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