title: Soluble egg antigen from Schistosoma japonicum modulates the progression of chronic progressive experimental autoimmune encephalomyelitis via Th2-shift response.
abstract: Soluble egg antigen (SEA) is strongly antigenic and inherently induces Th2-biased immune responses. In this study, we tested whether SEA from Schistosoma japonicum is able to prevent experimental autoimmune encephalomyelitis (EAE) induced by MOG(35-55) peptide, an established animal model of multiple sclerosis (MS). Intraperitoneal administration with SEA before EAE induction and in the preclinical phase after EAE induction successfully ameliorated the severity and progression of EAE on mice compared with phosphate buffered saline (PBS) controls, while no protective effect was shown when SEA immunization began after disease onset. This effect was associated with reduced interferon gamma (IFN-gamma) production and/or increased interleukin 4 (IL-4) production in spleen and central nervous system (CNS) even at the chronic stage. Similarly, we observed reduced inflammation and demyelination in spinal cords of SEA pretreated EAE mice compared with controls. Our data indicate that immunization with SEA from S. japonicum induces a preestablished Th2-biased microenvironment that provides preventive immune-modulating effects on EAE progression. This study may have important implications for its promising therapeutic use in MS and other autoimmune diseases.
authors.affiliation: Department of Neurology, the Third Affiliated Hospital of Sun Yat-Sen University, 600 Tianhe Road, Guangzhou, Guangdong 510630, China.
authors.forename: Xueping
authors.initials: X
authors.lastname: Zheng
authors.forename: Xueqiang
authors.initials: X
authors.lastname: Hu
authors.forename: Guoyu
authors.initials: G
authors.lastname: Zhou
authors.forename: Zhengqi
authors.initials: Z
authors.lastname: Lu
authors.forename: Wei
authors.initials: W
authors.lastname: Qiu
authors.forename: Jian
authors.initials: J
authors.lastname: Bao
authors.forename: Yongqiang
authors.initials: Y
authors.lastname: Dai
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D000947:Antigens, Helminth / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D002490:Central Nervous System / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D004334:Drug Administration Schedule; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D005260:Female; D006023:Glycoproteins / Q000276:immunology / Q000633:toxicity; D007155:Immunologic Factors / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D007274:Injections, Intraperitoneal; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments / Q000276:immunology / Q000633:toxicity; D012549:Schistosoma japonicum / Q000276:immunology*; D013154:Spleen / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology*
chemical_list: D000947:Antigens, Helminth; D006023:Glycoproteins; D007155:Immunologic Factors; D063308:Myelin-Oligodendrocyte Glycoprotein; D010446:Peptide Fragments; C445081:myelin oligodendrocyte glycoprotein (35-55); D015847:Interleukin-4; D007371:Interferon-gamma