title: The C-type lectin CD209b is expressed on microglia and it mediates the uptake of capsular polysaccharides of Streptococcus pneumoniae.
abstract: Although Streptococcus pneumoniae is the major cause of meningitis, how it causes disease is poorly understood. The C-type lectin SIGN-R1 mediates the recently described SIGN-R1 complement activation pathway, which operates against capsular polysaccharides (CPSs) of S. pneumoniae in splenic marginal macrophages. Here, we demonstrate that SIGN-R1, as well as the rat SIGN-R1 homologue CD209b are expressed in most regions of mouse or rat brain, respectively. Moreover, both C-type lectins are obviously expressed on microglia, but not on neurons or astrocytes. We also found that rat CD209b mediates the uptake of dextran or CPS14 within the rat splenic marginal zone, similar to SIGN-R1. On microglia, rat CD209b also mediates the uptake of CPS14 of S. pneumoniae. Our findings strongly suggest that both rat CD209b and SIGN-R1 on microglia mediate the SIGN-R1 complement activation pathway against S. pneumoniae, and thereby plays an important role in the pathogenesis of pneumococcal meningitis.
authors.affiliation: Department of Biomedical Science & Technology, Institute of Biomedical Science & Technology (IBST), Konkuk University, 1 Hwayang-dong, Kwangjin-gu, Seoul 143-701, Republic of Korea.
authors.forename: Jin-Yeon
authors.initials: JY
authors.lastname: Park
authors.forename: Heong-Jwa
authors.initials: HJ
authors.lastname: Choi
authors.forename: Miglena G V
authors.initials: MG
authors.lastname: Prabagar
authors.forename: Woo-Sung
authors.initials: WS
authors.lastname: Choi
authors.forename: Sun-Jong
authors.initials: SJ
authors.lastname: Kim
authors.forename: Cheolho
authors.initials: C
authors.lastname: Cheong
authors.forename: Chae Gyu
authors.initials: CG
authors.lastname: Park
authors.forename: Chan Young
authors.initials: CY
authors.lastname: Chin
authors.forename: Young-Sun
authors.initials: YS
authors.lastname: Kang
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D016667:Bacterial Capsules / Q000378:metabolism*; D001921:Brain / Q000378:metabolism* / Q000382:microbiology / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002478:Cells, Cultured; D003167:Complement Activation / Q000502:physiology; D005260:Female; D037181:Lectins, C-Type / Q000378:metabolism*; D008586:Meningitis, Pneumococcal / Q000378:metabolism / Q000503:physiopathology; D051379:Mice; D008807:Mice, Inbred BALB C; D017628:Microglia / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000378:metabolism*; D013296:Streptococcus pneumoniae / Q000378:metabolism*; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D037181:Lectins, C-Type; D011956:Receptors, Cell Surface; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C539982:Clec4m protein, rat