title: Mice lacking serum amyloid P component do not necessarily develop severe autoimmune disease.
abstract: Serum amyloid P component (SAP) is a major acute-phase reactant in mice. Recently, it was reported that SAP-deficient mice spontaneously developed anti-nuclear antibodies and severe glomerulonephritis. Because the SAP-deficient mice we generated display no obvious phenotypic abnormalities, we investigated whether our SAP-deficient mice would also spontaneously develop autoimmune responses. In accordance with the report, our mice produced high titers of anti-nuclear antibody but did not develop severe glomerulonephritis. On the other hand, it was recently reported that SAP bound to gram-negative bacteria via lipopolysaccharide (LPS) prevented LPS-mediated activation of a classical complement pathway. Thus, we asked if SAP-deficient mice would show altered responses to an intraperitoneal injection of LPS from Salmonella typhimirium. SAP-deficiency did afford resistance to lethality induced by high-dose LPS. Our experiments clearly showed that contrary to documented data, SAP-deficient mice do not develop serious autoimmune disease and we suggest that SAP has a critical role in LPS toxicity.
authors.affiliation: First Department of Biochemistry, Yamanashi Medical University, 1110 Shimokato, Tamaho-cho, Nakakoma-gun, Yamanashi 409-3898, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Soma
authors.forename: T
authors.initials: T
authors.lastname: Tamaoki
authors.forename: H
authors.initials: H
authors.lastname: Kawano
authors.forename: S
authors.initials: S
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Sakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: Y
authors.initials: Y
authors.lastname: Ozaki
authors.forename: S
authors.initials: S
authors.lastname: Kanba
authors.forename: Y
authors.initials: Y
authors.lastname: Hamada
authors.forename: T
authors.initials: T
authors.lastname: Ishihara
authors.forename: S
authors.initials: S
authors.lastname: Maeda
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics / Q000503:physiopathology*; D001483:Base Sequence; D017931:DNA Primers; D005260:Female; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012486:Salmonella typhimurium / Q000378:metabolism; D000683:Serum Amyloid P-Component / Q000235:genetics / Q000502:physiology*
chemical_list: D017931:DNA Primers; D008070:Lipopolysaccharides; D000683:Serum Amyloid P-Component