C-Phycocyanin ameliorates experimental autoimmune encephalomyelitis and induces regulatory T cells.
For decades Experimental Autoimmune Encephalitis (EAE) has remained as an unsurpassed multiple sclerosis (MS) animal model. C-Phycocyanin (C-Pc) has been reported to exhibit pharmacological properties that may be expected to symptomatically improve EAE and MS. However, in this paper we reveal a basic underlying mechanism that may provide a new approach to the rationale of the overall beneficial effect of this natural antioxidant. We demonstrate that C-Pc is able to trigger mechanisms preventing or downgrading EAE expression and induces a regulatory T cell (Treg) response, in peripheral blood mononuclear cells (PBMC) from MS patients. These results agree with reports suggesting that Treg limit acute MS attacks and that C-Pc may act as a neuroprotector and thereby reverts the organic and functional damage in neurodegenerative disorders of the central nervous system (CNS). Moreover, evidence is provided on the antioxidant activity of C-Pc within the CNS, intended to improve the myelin and axonal damage of EAE induced Lewis rats. Our results indicate that specific Treg activation may represent a central and essential mechanism in supporting the therapeutic potential of C-Pc for MS and may lead to new and more effective therapies; this property would then complement and enhance other proven active principles such as interferons (IFN), giving rise to combined therapies.
Pentón-Rol
Giselle
G
Center for Genetic Engineering and Biotechnology (CIGB), PO Box 6162, Havana, Cuba. giselle.penton@cigb.edu.cu
Martínez-Sánchez
Gregorio
G
Cervantes-Llanos
Majel
M
Lagumersindez-Denis
Nielsen
N
Acosta-Medina
Emilio Felino
EF
Falcón-Cama
Viviana
V
Alonso-Ramírez
Ruby
R
Valenzuela-Silva
Carmen
C
Rodríguez-Jiménez
Efraín
E
Llópiz-Arzuaga
Alexey
A
Marín-Prida
Javier
J
López-Saura
Pedro Antonio
PA
Guillén-Nieto
Gerardo Emilio
GE
Pentón-Arias
Eduardo
E
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000975:Antioxidants / Q000008:administration & dosage / Q000302:isolation & purification / Q000627:therapeutic use*; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D001921:Brain / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D002478:Cells, Cultured; D000458:Cyanobacteria / Q000737:chemistry; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000097:blood / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D005434:Flow Cytometry; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage / Q000627:therapeutic use; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D046529:Microscopy, Electron, Transmission; D009103:Multiple Sclerosis / Q000097:blood / Q000276:immunology; D010084:Oxidation-Reduction; D010798:Phycocyanin / Q000008:administration & dosage / Q000302:isolation & purification / Q000627:therapeutic use*; D051381:Rats; D011917:Rats, Inbred Lew; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D010798:Phycocyanin; D006854:Hydrocortisone