title: B1 cells produce nitric oxide in response to a series of toll-like receptor ligands.
abstract: The effect of a series of toll-like receptor (TLR) ligands on the production of nitric oxide (NO) in mouse B1 cells was examined by using CD5(+) IgM(+) WEHI 231 cells. The stimulation with a series of TLR ligands, which were Pam3Csk4 for TLR1/2, poly I:C for TLR3, lipopolysaccharide (LPS) for TLR4, imiquimod for TLR7 and CpG DNA for TLR9, resulted in enhanced NO production via augmented expression of an inducible type of NO synthase (iNOS). LPS was most potent for the enhancement of NO production, followed by poly I:C and Pam3Csk4. Imiquimod and CpG DNA led to slight NO production. The LPS-induced NO production was dependent on MyD88-dependent pathway consisting of nuclear factor (NF)-kappaB and a series of mitogen-activated protein kinases (MAPKs). Further, it was also dependent on the MyD88-independent pathway consisting of toll-IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) and interferon regulatory factor (IRF)-3. Physiologic peritoneal B1 cells also produced NO via the iNOS expression in response to LPS. The immunological significance of TLR ligands-induced NO production in B1 cells is discussed.
authors.affiliation: Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Japan.
authors.forename: Gantsetseg
authors.initials: G
authors.lastname: Tumurkhuu
authors.forename: Naoki
authors.initials: N
authors.lastname: Koide
authors.forename: Jargalsaikhan
authors.initials: J
authors.lastname: Dagvadorj
authors.forename: Abu S M
authors.initials: AS
authors.lastname: Noman
authors.forename: Imtiaz I-E
authors.initials: II
authors.lastname: Khuda
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Naiki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Komatsu
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Yoshida
authors.forename: Takashi
authors.initials: T
authors.lastname: Yokochi
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport / Q000235:genetics / Q000378:metabolism; D000634:Aminoquinolines / Q000378:metabolism; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D018956:CD5 Antigens / Q000378:metabolism; D002460:Cell Line; D004247:DNA / Q000378:metabolism; D005260:Female; D000077271:Imiquimod; D007075:Immunoglobulin M / Q000378:metabolism; D007369:Interferon Inducers / Q000378:metabolism; D008024:Ligands; D008070:Lipopolysaccharides / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D009838:Oligodeoxyribonucleotides / Q000235:genetics / Q000378:metabolism; D011070:Poly I-C / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D051193:Toll-Like Receptors / Q000378:metabolism*
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D000634:Aminoquinolines; D018956:CD5 Antigens; D004247:DNA; D000077271:Imiquimod; D007075:Immunoglobulin M; D007369:Interferon Inducers; D008024:Ligands; D008070:Lipopolysaccharides; D053594:Myeloid Differentiation Factor 88; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D009573:Nitrites; D009838:Oligodeoxyribonucleotides; D011070:Poly I-C; D051193:Toll-Like Receptors; C526836:Cd5 protein, mouse; C507780:Myd88 protein, mouse; C476286:Ticam1 protein, mouse