title: Inactivation of TLR9 by a suppressive oligodeoxynucleotides can ameliorate the clinical signs of EAN.
abstract: Susceptible-strain animals immunized with P2 peptide could generate the disease of experimental autoimmune neuritis (EAN) with inflammation and demyelination of peripheral nerve. A myriad of transcription factors and inflammatory cytokines have been found to participate in this process; however, the roles of toll-like receptors (TLRs) are poorly understood in EAN. The aim of this study is to explore the role of TLR9 in the pathogenesis of EAN. The EAN was induced in Lewis rat by immunization with P2(53-78) and complete Freund's adjuvant. CpG oligodeoxynucleotides (ODN) (cODN), a suppressive ODN (sODN) and a control non-specific ODN (nODN) were respectively administered to explore the role of TLR9 in EAN both in vivo and vitro. Following immunization up to the peak phase of EAN, EAN rats inoculated with sODN had remarkably better clinical score of EAN and expressed a significantly inhibited TLR9 signaling pathway. Our study suggests that TLR9 may be involved in the pathogenesis of EAN.
authors.affiliation: Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, PR China.
authors.forename: Yu-Zhong
authors.initials: YZ
authors.lastname: Wang
authors.forename: Qiu-Hua
authors.initials: QH
authors.lastname: Liang
authors.forename: Hhoonisha
authors.initials: H
authors.lastname: Ramkalawan
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Wen-Bin
authors.initials: WB
authors.lastname: Zhou
authors.forename: Bo
authors.initials: B
authors.lastname: Xiao
authors.forename: Fa-Fa
authors.initials: FF
authors.lastname: Tian
authors.forename: Huan
authors.initials: H
authors.lastname: Yang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ning-An
authors.initials: NA
authors.lastname: Xu
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D018450:Disease Progression; D004198:Disease Susceptibility; D005620:Freund's Adjuvant / Q000008:administration & dosage; D020275:Guillain-Barre Syndrome / Q000276:immunology* / Q000628:therapy; D006801:Humans; D007114:Immunization; D008297:Male; D018996:Myelin P2 Protein / Q000008:administration & dosage; D009444:Neuritis, Autoimmune, Experimental / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology / Q000628:therapy; D020319:Oligodeoxyribonucleotides, Antisense / Q000008:administration & dosage* / Q000009:adverse effects; D010446:Peptide Fragments / Q000008:administration & dosage; D051381:Rats; D011917:Rats, Inbred Lew; D051217:Toll-Like Receptor 9 / Q000235:genetics / Q000378:metabolism*
chemical_list: D018996:Myelin P2 Protein; D020319:Oligodeoxyribonucleotides, Antisense; D010446:Peptide Fragments; D051217:Toll-Like Receptor 9; C403271:myelin P2 protein (53-78); D005620:Freund's Adjuvant