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.
Center for Genetic Engineering and Biotechnology (CIGB), PO Box 6162, Havana, Cuba. giselle.penton@cigb.edu.cu
Giselle
G
Pentón-Rol
Gregorio
G
Martínez-Sánchez
Majel
M
Cervantes-Llanos
Nielsen
N
Lagumersindez-Denis
Emilio Felino
EF
Acosta-Medina
Viviana
V
Falcón-Cama
Ruby
R
Alonso-Ramírez
Carmen
C
Valenzuela-Silva
Efraín
E
Rodríguez-Jiménez
Alexey
A
Llópiz-Arzuaga
Javier
J
Marín-Prida
Pedro Antonio
PA
López-Saura
Gerardo Emilio
GE
Guillén-Nieto
Eduardo
E
Pentón-Arias
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