title: Expression of C1q, a subcomponent of the rat complement system, is dramatically enhanced in brains of rats with either Borna disease or experimental allergic encephalomyelitis.
abstract: In situ hybridization, RT-PCR and Northern blot analysis as well immunohistochemistry were used to examine the expression of C1q, a subcomponent of the rat complement system, in brains of rats infected with Borna disease virus (BDV) and rats afflicted with experimental allergic encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein specific T cells. C1q mRNA, which was not detected in normal brain, became clearly detectable using RT-PCR analysis by d14 post infection (p.i.) with BDV. Maximal levels of C1q mRNA were reached 21 days p.i. when inflammatory reactions in the brain were also at a peak. Similarly, C1q mRNA was elevated when the clinical symptoms of EAE became evident 5 days following cell transfer. C1q positive cells, as identified by immunohistology, were preferentially localized in grey and white matter of the hippocampus and basolateral cortex. The C1q positive cells resembled microglial cells in morphology. The correlation of C1q expression with the development of neurological disease as well as the dramatic increase of C1q within brain regions with inflammatory lesions suggest that local biosynthesis of C1q may play a role in the pathogenesis of Borna virus induced and autoimmune encephalomyelitis.
authors.affiliation: Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107-6799, USA.
authors.forename: B
authors.initials: B
authors.lastname: Dietzschold
authors.forename: W
authors.initials: W
authors.lastname: Schwaeble
authors.forename: M K
authors.initials: MK
authors.lastname: Schäfer
authors.forename: D C
authors.initials: DC
authors.lastname: Hooper
authors.forename: Y M
authors.initials: YM
authors.lastname: Zehng
authors.forename: F
authors.initials: F
authors.lastname: Petry
authors.forename: H
authors.initials: H
authors.lastname: Sheng
authors.forename: T
authors.initials: T
authors.lastname: Fink
authors.forename: M
authors.initials: M
authors.lastname: Loos
authors.forename: H
authors.initials: H
authors.lastname: Koprowski
authors.forename: E
authors.initials: E
authors.lastname: Weihe
mesh_terms: D000818:Animals; D001483:Base Sequence; D015152:Blotting, Northern; D015139:Blotting, Southern; D001890:Borna Disease / Q000378:metabolism* / Q000473:pathology; D001923:Brain Chemistry / Q000502:physiology*; D015922:Complement C1q / Q000096:biosynthesis*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D017628:Microglia / Q000378:metabolism; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D012194:RNA-Directed DNA Polymerase; D051381:Rats; D015854:Up-Regulation / Q000502:physiology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D015922:Complement C1q; D012194:RNA-Directed DNA Polymerase