Skip to main content
Erschienen in: Current Treatment Options in Neurology 4/2015

01.04.2015 | Multiple Sclerosis and Related Disorders (P Villoslada, Section Editor)

The Gut Microbiome in Multiple Sclerosis

verfasst von: Daniel W. Mielcarz, PhD, Lloyd H. Kasper, MD

Erschienen in: Current Treatment Options in Neurology | Ausgabe 4/2015

Einloggen, um Zugang zu erhalten

Opinion statement

The gut microbiome is made up of a wide range of (chiefly) bacterial species that colonize the small and large intestine. The human gut microbiome contains a subset of thousands of bacterial species, with up to 1014 total bacteria. Studies examining this bacterial content have shown wide variations in which species are present between individuals. The gut microbiome has been shown to have profound effects on the development and maintenance of immune system in both animal models and in humans. A growing body of evidence has implicated the human gut microbiome in a range of disorders, including obesity, inflammatory bowel diseases, and cardiovascular disease. Animal studies present compelling evidence that the gut microbiome plays a significant role in the progression of demyelinating disease, and that modulation of the microbiome can lead to either exacerbation or amelioration of symptoms. Differences in diet, vitamin D insufficiency, smoking, and alcohol use have all been implicated as risk factors in MS, and all have the ability to affect the composition of the gut microbiota. Preliminary clinical trials aimed at modulating the gut microbiota in MS patients are underway and may prove to be a promising and lower-risk treatment option in the future.
Literatur
1.
Zurück zum Zitat Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med. 2000;343:938–52.CrossRefPubMed Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG. Multiple sclerosis. N Engl J Med. 2000;343:938–52.CrossRefPubMed
2.
Zurück zum Zitat Weiner HL. The challenge of multiple sclerosis: how do we cure a chronic heterogeneous disease? Ann Neurol. 2009;65:239–48.CrossRefPubMed Weiner HL. The challenge of multiple sclerosis: how do we cure a chronic heterogeneous disease? Ann Neurol. 2009;65:239–48.CrossRefPubMed
3.
Zurück zum Zitat Krumbholz M, Derfuss T, Hohlfeld R, Meinl E. B cells and antibodies in multiple sclerosis pathogenesis and therapy. Nat Rev Neurol. 2012;8:13–623.CrossRef Krumbholz M, Derfuss T, Hohlfeld R, Meinl E. B cells and antibodies in multiple sclerosis pathogenesis and therapy. Nat Rev Neurol. 2012;8:13–623.CrossRef
4.
Zurück zum Zitat Fazekas F, Enzinger C, Wallner-Blazek M, Ropele S, Pluta-Fuerst A, Fuchs S. Gender differences in MRI studies on multiple sclerosis. J Neurol Sci. 2009;286:28–30.CrossRefPubMed Fazekas F, Enzinger C, Wallner-Blazek M, Ropele S, Pluta-Fuerst A, Fuchs S. Gender differences in MRI studies on multiple sclerosis. J Neurol Sci. 2009;286:28–30.CrossRefPubMed
7.
Zurück zum Zitat Oksenberg JR, Baranzini SE, Sawcer S, Hauser SL. The genetics of multiple sclerosis: SNPs to pathways to pathogenesis. Nat Rev Genet. 2008;9:516–26.CrossRefPubMed Oksenberg JR, Baranzini SE, Sawcer S, Hauser SL. The genetics of multiple sclerosis: SNPs to pathways to pathogenesis. Nat Rev Genet. 2008;9:516–26.CrossRefPubMed
8.•
Zurück zum Zitat International Multiple Sclerosis Genetics Consortium et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature. 2011;476:214–9. Study confirming several genetic factors associated with MS.CrossRef International Multiple Sclerosis Genetics Consortium et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature. 2011;476:214–9. Study confirming several genetic factors associated with MS.CrossRef
9.
Zurück zum Zitat Simpson Jr S, Blizzard L, Otahal P, Van der Mei I, Taylor B. Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis. J Neurol Neurosurg Psychiatry. 2011;82:1132–41.CrossRefPubMed Simpson Jr S, Blizzard L, Otahal P, Van der Mei I, Taylor B. Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis. J Neurol Neurosurg Psychiatry. 2011;82:1132–41.CrossRefPubMed
11.
Zurück zum Zitat Joscelyn J, Kasper LH. Digesting the emerging role for the gut microbiome in central nervous system demyelination. Mult Scler. 2014;20:1553–9.CrossRefPubMed Joscelyn J, Kasper LH. Digesting the emerging role for the gut microbiome in central nervous system demyelination. Mult Scler. 2014;20:1553–9.CrossRefPubMed
12.
Zurück zum Zitat Royal 3rd W, Mia Y, Li H, Naunton K. Peripheral blood regulatory T cell measurements correlate with serum vitamin D levels in patients with multiple sclerosis. J Neuroimmunol. 2009;213:135–41.CrossRefPubMed Royal 3rd W, Mia Y, Li H, Naunton K. Peripheral blood regulatory T cell measurements correlate with serum vitamin D levels in patients with multiple sclerosis. J Neuroimmunol. 2009;213:135–41.CrossRefPubMed
13.•
Zurück zum Zitat Kang SW et al. 1,25-dihyroxyvitamin D3 promotes FOXP3 expression via binding to vitamin D response elements in its conserved noncoding sequence region. J Immunol. 2012;188:5276–82. Evidence for role of Vitamin D in Treg function.CrossRefPubMedCentralPubMed Kang SW et al. 1,25-dihyroxyvitamin D3 promotes FOXP3 expression via binding to vitamin D response elements in its conserved noncoding sequence region. J Immunol. 2012;188:5276–82. Evidence for role of Vitamin D in Treg function.CrossRefPubMedCentralPubMed
14.
Zurück zum Zitat Matarese G et al. Leptin potentiates experimental autoimmune encephalomyelitis in SJL female mice and confers susceptibility to males. Eur J Immunol. 2001;31:1324–32.CrossRefPubMed Matarese G et al. Leptin potentiates experimental autoimmune encephalomyelitis in SJL female mice and confers susceptibility to males. Eur J Immunol. 2001;31:1324–32.CrossRefPubMed
15.
Zurück zum Zitat Matarese G et al. Requirement for leptin in the induction and progression of autoimmune encephalomyelitis. J Immunol. 2001;166:5909–16.CrossRefPubMed Matarese G et al. Requirement for leptin in the induction and progression of autoimmune encephalomyelitis. J Immunol. 2001;166:5909–16.CrossRefPubMed
16.
Zurück zum Zitat Lock C et al. Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. Nat Med. 2002;8:500–8.CrossRefPubMed Lock C et al. Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. Nat Med. 2002;8:500–8.CrossRefPubMed
17.
Zurück zum Zitat Matarese G et al. Leptin increase in multiple sclerosis associates with reduced number of CD4(+)CD25+ regulatory T cells. Proc Natl Acad Sci U S A. 2005;102:5150–5.CrossRefPubMedCentralPubMed Matarese G et al. Leptin increase in multiple sclerosis associates with reduced number of CD4(+)CD25+ regulatory T cells. Proc Natl Acad Sci U S A. 2005;102:5150–5.CrossRefPubMedCentralPubMed
18.
Zurück zum Zitat Sanna V, Di Giacomo A, La Cava A, Lechler RI, Fontana S, Zappacosta S, et al. Leptin surge precedes onset of autoimmune encephalomyelitis and correlates with development of pathogenic T cell responses. J Clin Invest. 2003;111:241–50.CrossRefPubMedCentralPubMed Sanna V, Di Giacomo A, La Cava A, Lechler RI, Fontana S, Zappacosta S, et al. Leptin surge precedes onset of autoimmune encephalomyelitis and correlates with development of pathogenic T cell responses. J Clin Invest. 2003;111:241–50.CrossRefPubMedCentralPubMed
20.•
Zurück zum Zitat Correale J. Helminth/parasite treatment of multiple sclerosis. Curr Treat Options Neurol. 2014;16:296. Review of Helminth treatment of MS, which is related to the gut microflora.CrossRefPubMed Correale J. Helminth/parasite treatment of multiple sclerosis. Curr Treat Options Neurol. 2014;16:296. Review of Helminth treatment of MS, which is related to the gut microflora.CrossRefPubMed
21.
Zurück zum Zitat Fabis Pedrini MJ, et al. Helicobacter pylori infection as a protective factor against multiple sclerosis risk in females. J Neurol Neurosurg Psychiatry. 2015. Fabis Pedrini MJ, et al. Helicobacter pylori infection as a protective factor against multiple sclerosis risk in females. J Neurol Neurosurg Psychiatry. 2015.
22.•
Zurück zum Zitat Wang Y, Kasper LH. The role of microbiome in central nervous system disorders. Brain Behav Immun. 2014;38:1–12. In depth review focusing on the microbiome and CNS disorders beyod MS.CrossRefPubMed Wang Y, Kasper LH. The role of microbiome in central nervous system disorders. Brain Behav Immun. 2014;38:1–12. In depth review focusing on the microbiome and CNS disorders beyod MS.CrossRefPubMed
23.
Zurück zum Zitat Ochoa-Reparaz J, Kasper LH. Gut microbiome and the risk factors in central nervous system autoimmunity. FEBS Lett. 2014;588:4214–22.CrossRefPubMed Ochoa-Reparaz J, Kasper LH. Gut microbiome and the risk factors in central nervous system autoimmunity. FEBS Lett. 2014;588:4214–22.CrossRefPubMed
24.•
Zurück zum Zitat Ley RE, Peterson DA, Gordon JI. Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell. 2006;124:837–48. Gut microbiota can exacerbate EAE.CrossRefPubMed Ley RE, Peterson DA, Gordon JI. Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell. 2006;124:837–48. Gut microbiota can exacerbate EAE.CrossRefPubMed
25.
Zurück zum Zitat Lee YK, Menezes JS, Umesaki Y, Mazmanian SK. Proinflammatory T-cell responses to gut microbiota promote experimental autoimmune encephalomyelitis. Proc Natl Acad Sci U S A. 2011;108 Suppl 1:4615–22.CrossRefPubMedCentralPubMed Lee YK, Menezes JS, Umesaki Y, Mazmanian SK. Proinflammatory T-cell responses to gut microbiota promote experimental autoimmune encephalomyelitis. Proc Natl Acad Sci U S A. 2011;108 Suppl 1:4615–22.CrossRefPubMedCentralPubMed
26.
Zurück zum Zitat Berer K, Mues M, Koutrolos M, Rasbi ZA, Boziki M, Johner C, et al. Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Nature. 2011;479:538–41.CrossRefPubMed Berer K, Mues M, Koutrolos M, Rasbi ZA, Boziki M, Johner C, et al. Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Nature. 2011;479:538–41.CrossRefPubMed
27.••
Zurück zum Zitat Ochoa-Reparaz J, Mielcarz DW, Ditrio LE, Burroughs AR, Foureau DM, Haque-Begum S, et al. Role of gut commensal microflora in the development of experimental autoimmune encephalomyelitis. J Immunol. 2009;183:6041–50. Antibiotic treatment prevents EAE induction, and gut microflora reconstitution enables it.CrossRefPubMed Ochoa-Reparaz J, Mielcarz DW, Ditrio LE, Burroughs AR, Foureau DM, Haque-Begum S, et al. Role of gut commensal microflora in the development of experimental autoimmune encephalomyelitis. J Immunol. 2009;183:6041–50. Antibiotic treatment prevents EAE induction, and gut microflora reconstitution enables it.CrossRefPubMed
28.
Zurück zum Zitat Yokote H, Miyake S, Croxford JL, Oki S, Mizusawa H, Yamamura T. NKT cell-dependent amelioration of a mouse model of multiple sclerosis by altering gut flora. Am J Pathol. 2008;173:1714–23.CrossRefPubMedCentralPubMed Yokote H, Miyake S, Croxford JL, Oki S, Mizusawa H, Yamamura T. NKT cell-dependent amelioration of a mouse model of multiple sclerosis by altering gut flora. Am J Pathol. 2008;173:1714–23.CrossRefPubMedCentralPubMed
29.••
Zurück zum Zitat Ochoa-Reparaz J, Mielcarz DW, Ditrio LE, Burroughs AR, Begum-Haque S, Dasgupta S, et al. Central nervous system demyelinating disease protection by the human commensal Bacteroides fragilis depends on polysaccharide A expression. J Immunol. 2010;185:4101–8. Demonstrates that a single polysaccharide from a member of the gut microflora can protect against EAE.CrossRefPubMed Ochoa-Reparaz J, Mielcarz DW, Ditrio LE, Burroughs AR, Begum-Haque S, Dasgupta S, et al. Central nervous system demyelinating disease protection by the human commensal Bacteroides fragilis depends on polysaccharide A expression. J Immunol. 2010;185:4101–8. Demonstrates that a single polysaccharide from a member of the gut microflora can protect against EAE.CrossRefPubMed
30.
Zurück zum Zitat Ochoa-Reparaz J, Mielcarz DW, Haque-Begum S, Kasper LH. Induction of a regulatory B cell population in experimental allergic encephalomyelitis by alteration of the gut commensal microflora. Gut Microbes. 2010;1:103–8.CrossRefPubMedCentralPubMed Ochoa-Reparaz J, Mielcarz DW, Haque-Begum S, Kasper LH. Induction of a regulatory B cell population in experimental allergic encephalomyelitis by alteration of the gut commensal microflora. Gut Microbes. 2010;1:103–8.CrossRefPubMedCentralPubMed
31.
Zurück zum Zitat Ochoa-Reparaz J, Mielcarz DW, Wang Y, Begum-Haque S, Dasgupta S, Kasper DL, et al. A polysaccharide from the human commensal Bacteroides fragilis protects against CNS demyelinating disease. Mucosal Immunol. 2010;3:487–95.CrossRefPubMed Ochoa-Reparaz J, Mielcarz DW, Wang Y, Begum-Haque S, Dasgupta S, Kasper DL, et al. A polysaccharide from the human commensal Bacteroides fragilis protects against CNS demyelinating disease. Mucosal Immunol. 2010;3:487–95.CrossRefPubMed
32.
Zurück zum Zitat Wang Y et al. An intestinal commensal symbiosis factor controls neuroinflammation via TLR2-mediated CD39 signalling. Nat Commun. 2014;5:4432.PubMedCentralPubMed Wang Y et al. An intestinal commensal symbiosis factor controls neuroinflammation via TLR2-mediated CD39 signalling. Nat Commun. 2014;5:4432.PubMedCentralPubMed
33.
Zurück zum Zitat Wang Y et al. A commensal bacterial product elicits and modulates migratory capacity of CD39(+) CD4 T regulatory subsets in the suppression of neuroinflammation. Gut Microbes. 2014;5:552–61.CrossRefPubMed Wang Y et al. A commensal bacterial product elicits and modulates migratory capacity of CD39(+) CD4 T regulatory subsets in the suppression of neuroinflammation. Gut Microbes. 2014;5:552–61.CrossRefPubMed
34.
Zurück zum Zitat Jun S, Ochoa-Reparaz J, Zlotkowska D, Hoyt T, Pascual DW. Bystander-mediated stimulation of proteolipid protein-specific regulatory T (Treg) cells confers protection against experimental autoimmune encephalomyelitis (EAE) via TGF-beta. J Neuroimmunol. 2012;245:39–47.CrossRefPubMedCentralPubMed Jun S, Ochoa-Reparaz J, Zlotkowska D, Hoyt T, Pascual DW. Bystander-mediated stimulation of proteolipid protein-specific regulatory T (Treg) cells confers protection against experimental autoimmune encephalomyelitis (EAE) via TGF-beta. J Neuroimmunol. 2012;245:39–47.CrossRefPubMedCentralPubMed
35.
Zurück zum Zitat Ochoa-Reparaz J, Riccardi C, Rynda A, Jun S, Callis G, Pascual DW. Regulatory T cell vaccination without autoantigen protects against experimental autoimmune encephalomyelitis. J Immunol. 2007;178:1791–9.CrossRefPubMed Ochoa-Reparaz J, Riccardi C, Rynda A, Jun S, Callis G, Pascual DW. Regulatory T cell vaccination without autoantigen protects against experimental autoimmune encephalomyelitis. J Immunol. 2007;178:1791–9.CrossRefPubMed
36.
Zurück zum Zitat Jun S, Gilmore W, Callis G, Rynda A, Haddad A, Pascual DW. A live diarrheal vaccine imprints a Th2 cell bias and acts as an anti-inflammatory vaccine. J Immunol. 2005;175:6733–40.CrossRefPubMed Jun S, Gilmore W, Callis G, Rynda A, Haddad A, Pascual DW. A live diarrheal vaccine imprints a Th2 cell bias and acts as an anti-inflammatory vaccine. J Immunol. 2005;175:6733–40.CrossRefPubMed
37.
Zurück zum Zitat Ezendam J, de Klerk A, Gremmer ER, van Loveren H. Effects of Bifidobacterium animalis administered during lactation on allergic and autoimmune responses in rodents. Clin Exp Immunol. 2008;154:424–31.CrossRefPubMedCentralPubMed Ezendam J, de Klerk A, Gremmer ER, van Loveren H. Effects of Bifidobacterium animalis administered during lactation on allergic and autoimmune responses in rodents. Clin Exp Immunol. 2008;154:424–31.CrossRefPubMedCentralPubMed
38.
Zurück zum Zitat Lavasani S et al. A novel probiotic mixture exerts a therapeutic effect on experimental autoimmune encephalomyelitis mediated by IL-10 producing regulatory T cells. PLoS ONE. 2010;5:e9009.CrossRefPubMedCentralPubMed Lavasani S et al. A novel probiotic mixture exerts a therapeutic effect on experimental autoimmune encephalomyelitis mediated by IL-10 producing regulatory T cells. PLoS ONE. 2010;5:e9009.CrossRefPubMedCentralPubMed
39.
Zurück zum Zitat Takata K et al. The lactic acid bacterium Pediococcus acidilactici suppresses autoimmune encephalomyelitis by inducing IL-10-producing regulatory T cells. PLoS ONE. 2011;6:e27644.CrossRefPubMedCentralPubMed Takata K et al. The lactic acid bacterium Pediococcus acidilactici suppresses autoimmune encephalomyelitis by inducing IL-10-producing regulatory T cells. PLoS ONE. 2011;6:e27644.CrossRefPubMedCentralPubMed
40.
Zurück zum Zitat Maassen CB, Claassen E. Strain-dependent effects of probiotic lactobacilli on EAE autoimmunity. Vaccine. 2008;26:2056–7.CrossRefPubMed Maassen CB, Claassen E. Strain-dependent effects of probiotic lactobacilli on EAE autoimmunity. Vaccine. 2008;26:2056–7.CrossRefPubMed
41.
Zurück zum Zitat Kwon HK et al. Amelioration of experimental autoimmune encephalomyelitis by probiotic mixture is mediated by a shift in T helper cell immune response. Clin Immunol. 2013;146:217–27.CrossRefPubMed Kwon HK et al. Amelioration of experimental autoimmune encephalomyelitis by probiotic mixture is mediated by a shift in T helper cell immune response. Clin Immunol. 2013;146:217–27.CrossRefPubMed
42.
Zurück zum Zitat Rezende RM et al. Hsp65-producing Lactococcus lactis prevents experimental autoimmune encephalomyelitis in mice by inducing CD4+LAP+ regulatory T cells. J Autoimmun. 2013;40:45–57.CrossRefPubMedCentralPubMed Rezende RM et al. Hsp65-producing Lactococcus lactis prevents experimental autoimmune encephalomyelitis in mice by inducing CD4+LAP+ regulatory T cells. J Autoimmun. 2013;40:45–57.CrossRefPubMedCentralPubMed
43.••
Zurück zum Zitat Hooper LV, Littman DR, Macpherson AJ. Interactions between the microbiota and the immune system. Science. 2012;336:1268–73. Excellent review on the manners in which the gut microbiota and immune system interact.CrossRefPubMed Hooper LV, Littman DR, Macpherson AJ. Interactions between the microbiota and the immune system. Science. 2012;336:1268–73. Excellent review on the manners in which the gut microbiota and immune system interact.CrossRefPubMed
44.
Zurück zum Zitat Macpherson AJ, Harris NL. Interactions between commensal intestinal bacteria and the immune system. Nat Rev Immunol. 2004;4:478–85.CrossRefPubMed Macpherson AJ, Harris NL. Interactions between commensal intestinal bacteria and the immune system. Nat Rev Immunol. 2004;4:478–85.CrossRefPubMed
45.
Zurück zum Zitat Mackie RI, Sghir A, Gaskins HR. Developmental microbial ecology of the neonatal gastrointestinal tract. Am J Clin Nutr. 1999;69:1035S–45.PubMed Mackie RI, Sghir A, Gaskins HR. Developmental microbial ecology of the neonatal gastrointestinal tract. Am J Clin Nutr. 1999;69:1035S–45.PubMed
47.
Zurück zum Zitat Begum-Haque S, Christy M, Ochoa-Reparaz J, Nowak EC, Mielcarz D, Haque A, et al. Augmentation of regulatory B cell activity in experimental allergic encephalomyelitis by glatiramer acetate. J Neuroimmunol. 2011;232:136–44.CrossRefPubMedCentralPubMed Begum-Haque S, Christy M, Ochoa-Reparaz J, Nowak EC, Mielcarz D, Haque A, et al. Augmentation of regulatory B cell activity in experimental allergic encephalomyelitis by glatiramer acetate. J Neuroimmunol. 2011;232:136–44.CrossRefPubMedCentralPubMed
48.
Zurück zum Zitat Tzianabos AO, Kasper DL, Onderdonk AB. Structure and function of Bacteroides fragilis capsular polysaccharides: relationship to induction and prevention of abscesses. Clin Infect Dis. 1995;20 Suppl 2:S132–40.CrossRefPubMed Tzianabos AO, Kasper DL, Onderdonk AB. Structure and function of Bacteroides fragilis capsular polysaccharides: relationship to induction and prevention of abscesses. Clin Infect Dis. 1995;20 Suppl 2:S132–40.CrossRefPubMed
49.
Zurück zum Zitat Pantosti A, Tzianabos AO, Reinap BG, Onderdonk AB, Kasper DL. Bacteroides fragilis strains express multiple capsular polysaccharides. J Clin Microbiol. 1993;31:1850–5.PubMedCentralPubMed Pantosti A, Tzianabos AO, Reinap BG, Onderdonk AB, Kasper DL. Bacteroides fragilis strains express multiple capsular polysaccharides. J Clin Microbiol. 1993;31:1850–5.PubMedCentralPubMed
50.
Zurück zum Zitat Mazmanian SK, Liu CH, Tzianabos AO, Kasper DL. An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system. Cell. 2005;122:107–18.CrossRefPubMed Mazmanian SK, Liu CH, Tzianabos AO, Kasper DL. An immunomodulatory molecule of symbiotic bacteria directs maturation of the host immune system. Cell. 2005;122:107–18.CrossRefPubMed
51.
Zurück zum Zitat Mazmanian SK, Kasper DL. The love-hate relationship between bacterial polysaccharides and the host immune system. Nat Rev Immunol. 2006;6:849–58.CrossRefPubMed Mazmanian SK, Kasper DL. The love-hate relationship between bacterial polysaccharides and the host immune system. Nat Rev Immunol. 2006;6:849–58.CrossRefPubMed
52.
Zurück zum Zitat Mazmanian SK, Round JL, Kasper DL. A microbial symbiosis factor prevents intestinal inflammatory disease. Nature. 2008;453:620–5.CrossRefPubMed Mazmanian SK, Round JL, Kasper DL. A microbial symbiosis factor prevents intestinal inflammatory disease. Nature. 2008;453:620–5.CrossRefPubMed
53.
Zurück zum Zitat Mazmanian SK. Capsular polysaccharides of symbiotic bacteria modulate immune responses during experimental colitis. J Pediatr Gastroenterol Nutr. 2008;46 Suppl 1:E11–2.CrossRefPubMed Mazmanian SK. Capsular polysaccharides of symbiotic bacteria modulate immune responses during experimental colitis. J Pediatr Gastroenterol Nutr. 2008;46 Suppl 1:E11–2.CrossRefPubMed
54.
Zurück zum Zitat Round JL, Lee SM, Li J, Tran G, Jabri B, Chatila TA, et al. The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota. Science. 2011;332:974–7.CrossRefPubMedCentralPubMed Round JL, Lee SM, Li J, Tran G, Jabri B, Chatila TA, et al. The Toll-like receptor 2 pathway establishes colonization by a commensal of the human microbiota. Science. 2011;332:974–7.CrossRefPubMedCentralPubMed
55.
Zurück zum Zitat Ochoa-Reparaz J et al. IL-13 production by regulatory T cells protects against experimental autoimmune encephalomyelitis independently of autoantigen. J Immunol. 2008;181:954–68.CrossRefPubMedCentralPubMed Ochoa-Reparaz J et al. IL-13 production by regulatory T cells protects against experimental autoimmune encephalomyelitis independently of autoantigen. J Immunol. 2008;181:954–68.CrossRefPubMedCentralPubMed
56.
Zurück zum Zitat Kochetkova I, Trunkle T, Callis G, Pascual DW. Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. J Immunol. 2008;181:2741–52.CrossRefPubMedCentralPubMed Kochetkova I, Trunkle T, Callis G, Pascual DW. Vaccination without autoantigen protects against collagen II-induced arthritis via immune deviation and regulatory T cells. J Immunol. 2008;181:2741–52.CrossRefPubMedCentralPubMed
57.
Zurück zum Zitat Mowry E, Waubant E, Chehoud C, DeSantis T, Kuczynski J, Warrington J. Gut bacterial populations in multiple sclerosis and in health (P05.106). Neurology. 2012;78:P05.106. Mowry E, Waubant E, Chehoud C, DeSantis T, Kuczynski J, Warrington J. Gut bacterial populations in multiple sclerosis and in health (P05.106). Neurology. 2012;78:P05.106.
58.
Zurück zum Zitat Bhargava P, Mowry EM. Gut microbiome and multiple sclerosis. Curr Neurol Neurosci Rep. 2014;14:492.CrossRefPubMed Bhargava P, Mowry EM. Gut microbiome and multiple sclerosis. Curr Neurol Neurosci Rep. 2014;14:492.CrossRefPubMed
59.
Zurück zum Zitat Rumah KR, Linden J, Fischetti VA, Vartanian T. Isolation of Clostridium perfringens type B in an individual at first clinical presentation of multiple sclerosis provides clues for environmental triggers of the disease. PLoS ONE. 2013;8:e76359.CrossRefPubMedCentralPubMed Rumah KR, Linden J, Fischetti VA, Vartanian T. Isolation of Clostridium perfringens type B in an individual at first clinical presentation of multiple sclerosis provides clues for environmental triggers of the disease. PLoS ONE. 2013;8:e76359.CrossRefPubMedCentralPubMed
60.•
Zurück zum Zitat Jhangi S et al. Increased Archaea species and changes with therapy in gut microbiome of multiple sclerosis subjects (S24.001). Neurology. 2014;82:S24.001. Largest study to date on the gut microbiome content of MS patients. Jhangi S et al. Increased Archaea species and changes with therapy in gut microbiome of multiple sclerosis subjects (S24.001). Neurology. 2014;82:S24.001. Largest study to date on the gut microbiome content of MS patients.
61.
Zurück zum Zitat Tremlett H et al. Gut microbiome in early pediatric multiple sclerosis: a case-control study. Mult Scler. 2014;20:285–496.CrossRef Tremlett H et al. Gut microbiome in early pediatric multiple sclerosis: a case-control study. Mult Scler. 2014;20:285–496.CrossRef
62.
Zurück zum Zitat Telesford K, Wang Y, Ochoa-Reparaz J, Begum-Haque S, Kasper LH. Commensal antigen induction of suppressive human Foxp3+ Tregs. Mult Scler. 2014;20:285–496.CrossRef Telesford K, Wang Y, Ochoa-Reparaz J, Begum-Haque S, Kasper LH. Commensal antigen induction of suppressive human Foxp3+ Tregs. Mult Scler. 2014;20:285–496.CrossRef
63.
Zurück zum Zitat Saemann MD et al. Anti-inflammatory effects of sodium butyrate on human monocytes: potent inhibition of IL-12 and up-regulation of IL-10 production. FASEB J. 2000;14:2380–2.PubMed Saemann MD et al. Anti-inflammatory effects of sodium butyrate on human monocytes: potent inhibition of IL-12 and up-regulation of IL-10 production. FASEB J. 2000;14:2380–2.PubMed
64.
Zurück zum Zitat Kampman MT, Brustad M. Vitamin D: a candidate for the environmental effect in multiple sclerosis—observations from Norway. Neuroepidemiology. 2008;30:140–6.CrossRefPubMed Kampman MT, Brustad M. Vitamin D: a candidate for the environmental effect in multiple sclerosis—observations from Norway. Neuroepidemiology. 2008;30:140–6.CrossRefPubMed
65.
Zurück zum Zitat Ly NP, Litonjua A, Gold DR, Celedon JC. Gut microbiota, probiotics, and vitamin D: interrelated exposures influencing allergy, asthma, and obesity? J Allergy Clin Immunol. 2011;127:1087–94. quiz 1095-6. Ly NP, Litonjua A, Gold DR, Celedon JC. Gut microbiota, probiotics, and vitamin D: interrelated exposures influencing allergy, asthma, and obesity? J Allergy Clin Immunol. 2011;127:1087–94. quiz 1095-6.
66.
Zurück zum Zitat Mai V, McCrary QM, Sinha R, Glei M. Associations between dietary habits and body mass index with gut microbiota composition and fecal water genotoxicity: an observational study in African American and Caucasian American volunteers. Nutr J. 2009;8:49.CrossRefPubMedCentralPubMed Mai V, McCrary QM, Sinha R, Glei M. Associations between dietary habits and body mass index with gut microbiota composition and fecal water genotoxicity: an observational study in African American and Caucasian American volunteers. Nutr J. 2009;8:49.CrossRefPubMedCentralPubMed
67.
Zurück zum Zitat Pozuelo-Moyano B, Benito-Leon J, Mitchell AJ, Hernandez-Gallego J. A systematic review of randomized, double-blind, placebo-controlled trials examining the clinical efficacy of vitamin D in multiple sclerosis. Neuroepidemiology. 2013;40:147–53.CrossRefPubMedCentralPubMed Pozuelo-Moyano B, Benito-Leon J, Mitchell AJ, Hernandez-Gallego J. A systematic review of randomized, double-blind, placebo-controlled trials examining the clinical efficacy of vitamin D in multiple sclerosis. Neuroepidemiology. 2013;40:147–53.CrossRefPubMedCentralPubMed
70.
71.
Zurück zum Zitat Tripathy D, Mohanty P, Dhindsa S, Syed T, Ghanim H, Aljada A, et al. Elevation of free fatty acids induces inflammation and impairs vascular reactivity in healthy subjects. Diabetes. 2003;52:2882–7.CrossRefPubMed Tripathy D, Mohanty P, Dhindsa S, Syed T, Ghanim H, Aljada A, et al. Elevation of free fatty acids induces inflammation and impairs vascular reactivity in healthy subjects. Diabetes. 2003;52:2882–7.CrossRefPubMed
Metadaten
Titel
The Gut Microbiome in Multiple Sclerosis
verfasst von
Daniel W. Mielcarz, PhD
Lloyd H. Kasper, MD
Publikationsdatum
01.04.2015
Verlag
Springer US
Erschienen in
Current Treatment Options in Neurology / Ausgabe 4/2015
Print ISSN: 1092-8480
Elektronische ISSN: 1534-3138
DOI
https://doi.org/10.1007/s11940-015-0344-7

Weitere Artikel der Ausgabe 4/2015

Current Treatment Options in Neurology 4/2015 Zur Ausgabe

Neurologic Ophthalmology and Otology (RK Shin and DR Gold, Section Editors)

Treatment of Menière’s Disease

Epilepsy (E Waterhouse, Section Editor)

Seizures in Setting of Dementia

Multiple Sclerosis and Related Disorders (P Villoslada, Section Editor)

Therapeutic Management of Severe Relapses in Multiple Sclerosis

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Frühe Alzheimertherapie lohnt sich

25.04.2024 AAN-Jahrestagung 2024 Nachrichten

Ist die Tau-Last noch gering, scheint der Vorteil von Lecanemab besonders groß zu sein. Und beginnen Erkrankte verzögert mit der Behandlung, erreichen sie nicht mehr die kognitive Leistung wie bei einem früheren Start. Darauf deuten neue Analysen der Phase-3-Studie Clarity AD.

Viel Bewegung in der Parkinsonforschung

25.04.2024 Parkinson-Krankheit Nachrichten

Neue arznei- und zellbasierte Ansätze, Frühdiagnose mit Bewegungssensoren, Rückenmarkstimulation gegen Gehblockaden – in der Parkinsonforschung tut sich einiges. Auf dem Deutschen Parkinsonkongress ging es auch viel um technische Innovationen.

Demenzkranke durch Antipsychotika vielfach gefährdet

23.04.2024 Demenz Nachrichten

Wenn Demenzkranke aufgrund von Symptomen wie Agitation oder Aggressivität mit Antipsychotika behandelt werden, sind damit offenbar noch mehr Risiken verbunden als bislang angenommen.

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.