
Contributions
Abstract: P1087
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Environmental factors
Background: Gut microbiota has been related to multiple sclerosis (MS) etiopathogenesis. Short-chain fatty acids (SCFA) are compounds derived from microbial metabolism that have a role in gut-brain axis. The most abundant SCFA are butyrate, propionate and acetate.
Objectives: To analyse SCFA plasma levels of MS patients and healthy donors (HD), and a possible link between these levels and both clinical characteristics of the pathology and immune cells populations.
Methods: 97 MS patients and 55 HD were included in this study. Patients were divided into two groups according to their EDSS (Expanded Disability Status Score), 50 with EDSS≤1.5 and 47 with EDSS≥5.0. Plasma samples were collected in order to analyse SCFA levels by liquid chromatography-mass spectrometry, and peripheral blood cells were isolated for flow cytometry analysis of immune cells populations.
Results: Acetate plasma levels were significantly higher in patients than in HD (p=0.002). Patients with EDSS≥5.0 had significantly higher acetate levels than those with EDSS≤1.5 (p=0.02), and than HD (p=1.79e-4), existing a correlation between acetate levels and EDSS (r=0.406, p=4.09e-5). In MS patients, every SCFA were correlated (propionate-acetate: r=0.443, p=6.81e-6; butyrate-acetate: r=0.315, p=0.002; propionate-butyrate: r=0.715, p=3.82e-16). Relating to flow cytometry analysis, the main associations were that MS patients with high acetate levels showed decreased CD4+ naïve T cells (r=-0.550, p=0.001) and increased CD8+ IL-17+ cells (r=0.556 p=0.001). In HD we did not find these associations, but high levels of propionate involved decreased B cells (r=-0.773, p=4.43e-4) and increased monocytes (r=0.613, p=0.001).
Conclusions: Acetate plasma levels are higher in MS patients than in HD. There exists a direct correlation between acetate plasma levels and EDSS in MS patients. In addition, high acetate levels seems to activate immune system in MS patients, favouring a Th17 response. Further studies are required to elucidate the mechanisms through which they could take part in the disease.
Disclosure: S. Pérez-Pérez: nothing to disclose.
M.I. Domínguez-Mozo: nothing to disclose.
S. Medina: nothing to disclose.
N. Villarubia: nothing to disclose.
A. Alonso-Gómez: nothing to disclose
M.A. García-Martínez: nothing to disclose.
L. Costa-Frossard: reports grants, personal fees and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec and Roche
J.C. Álvarez-Cermeño: reports grants, personal fees and non-financial support from Bayer Schering, Biogen Idec, Genzyme, Novartis, Merck-Serono, Roche, Sanofi-Aventis and Teva
R. Arroyo: received honoraria for speaking and participating as investigators in clinical trials and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec, Roche and Bayer-Schering.
L.M. Villar: reports grants, personal fees and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec and Roche
R. Álvarez-Lafuente: reports grants and personal fees from Merck-Serono, personal fees and non-financial support from Biogen IDEC, grants, personal fees and non-financial support from Novartis Pharmaceuticals S.A., grants and personal fees from Genzyme, non-financial support from TEVA Pharma, S.L., non-financial support from Roche.
Abstract: P1087
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Environmental factors
Background: Gut microbiota has been related to multiple sclerosis (MS) etiopathogenesis. Short-chain fatty acids (SCFA) are compounds derived from microbial metabolism that have a role in gut-brain axis. The most abundant SCFA are butyrate, propionate and acetate.
Objectives: To analyse SCFA plasma levels of MS patients and healthy donors (HD), and a possible link between these levels and both clinical characteristics of the pathology and immune cells populations.
Methods: 97 MS patients and 55 HD were included in this study. Patients were divided into two groups according to their EDSS (Expanded Disability Status Score), 50 with EDSS≤1.5 and 47 with EDSS≥5.0. Plasma samples were collected in order to analyse SCFA levels by liquid chromatography-mass spectrometry, and peripheral blood cells were isolated for flow cytometry analysis of immune cells populations.
Results: Acetate plasma levels were significantly higher in patients than in HD (p=0.002). Patients with EDSS≥5.0 had significantly higher acetate levels than those with EDSS≤1.5 (p=0.02), and than HD (p=1.79e-4), existing a correlation between acetate levels and EDSS (r=0.406, p=4.09e-5). In MS patients, every SCFA were correlated (propionate-acetate: r=0.443, p=6.81e-6; butyrate-acetate: r=0.315, p=0.002; propionate-butyrate: r=0.715, p=3.82e-16). Relating to flow cytometry analysis, the main associations were that MS patients with high acetate levels showed decreased CD4+ naïve T cells (r=-0.550, p=0.001) and increased CD8+ IL-17+ cells (r=0.556 p=0.001). In HD we did not find these associations, but high levels of propionate involved decreased B cells (r=-0.773, p=4.43e-4) and increased monocytes (r=0.613, p=0.001).
Conclusions: Acetate plasma levels are higher in MS patients than in HD. There exists a direct correlation between acetate plasma levels and EDSS in MS patients. In addition, high acetate levels seems to activate immune system in MS patients, favouring a Th17 response. Further studies are required to elucidate the mechanisms through which they could take part in the disease.
Disclosure: S. Pérez-Pérez: nothing to disclose.
M.I. Domínguez-Mozo: nothing to disclose.
S. Medina: nothing to disclose.
N. Villarubia: nothing to disclose.
A. Alonso-Gómez: nothing to disclose
M.A. García-Martínez: nothing to disclose.
L. Costa-Frossard: reports grants, personal fees and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec and Roche
J.C. Álvarez-Cermeño: reports grants, personal fees and non-financial support from Bayer Schering, Biogen Idec, Genzyme, Novartis, Merck-Serono, Roche, Sanofi-Aventis and Teva
R. Arroyo: received honoraria for speaking and participating as investigators in clinical trials and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec, Roche and Bayer-Schering.
L.M. Villar: reports grants, personal fees and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec and Roche
R. Álvarez-Lafuente: reports grants and personal fees from Merck-Serono, personal fees and non-financial support from Biogen IDEC, grants, personal fees and non-financial support from Novartis Pharmaceuticals S.A., grants and personal fees from Genzyme, non-financial support from TEVA Pharma, S.L., non-financial support from Roche.