title: Development of pristane induced mice model for lupus with atherosclerosis and analysis of TLR expression.
abstract: This study was designed to establish a murine model of lupus with atherosclerosis, and to investigate the expression of Toll-like receptors (TLRs) in the aorta and kidney.
  
  
  
  The 9-week-old female ApoE-/- and C57BL/6 mice were randomly divided into a ApoE-/- pristane treated group (group A), ApoE-/- control group (group B), C57BL/6 pristane treated group (group C) and C57BL/6 control group (group D). Each mouse was given either a single intraperitoneal injection of 0.5 ml pristane or saline.
  
  
  
  We observed that group A mice specifically had poor spirit, less activity, obvious hair loss, splenomegalia and renomegaly. Levels of ANA, anti-ds-DNA and anti-Sm antibodies were significantly higher than those in other groups. The group A and B mice generally displayed intimal hyperplasia and atherosclerosis mottling in the lumen of the aorta. The kidney tissues from group A, B and C mice showed increased expression levels of TLR2, TLR4, TLR7 and TLR9 proteins in comparison to group D. However, Group A mice did not show any significant difference in TLR2 and TLR4 protein expression levels when compared to group B and C, but displayed higher TLR7 expression than group B and higher TLR9 expression than group B and C mice. In contrast, the group A and B mice apparently expressed TLR2 and TLR4.
  
  
  
  We concluded that pristane treated apoE-/- mice exhibited lupus-like phenotype and developed atherosclerosis. The pristane treatment also induced abnormally high expression of TLR2 and TLR4 in the aorta and TLR2, TLR4, TLR7 and TLR9 in the kidney of apoE-/- mice.
authors.affiliation: Department of Rheumatology and Immunology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, China. qzlinl@163.com.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Rheumatology and Immunology, Xiamen 174 Hospital, China.
authors.forename: RanRan
authors.initials: R
authors.lastname: Cui
authors.affiliation: Department of Rheumatology and Immunology, Jingzhou City Central Hospital, China.
authors.forename: Rongda
authors.initials: R
authors.lastname: Li
authors.affiliation: Deparment of Vasculocardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
authors.forename: Huili
authors.initials: H
authors.lastname: Lin
authors.affiliation: Deparment of Vasculocardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
authors.forename: Ziyang
authors.initials: Z
authors.lastname: Huang
authors.affiliation: Department of Rheumatology and Immunology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Lin
mesh_terms: D000818:Animals; D001011:Aorta / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001018:Aortic Diseases / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D050197:Atherosclerosis / Q000139:chemically induced / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D007668:Kidney / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000139:chemically induced / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010641:Phenotype; D013729:Terpenes; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism*
chemical_list: D001057:Apolipoproteins E; D013729:Terpenes; D051193:Toll-Like Receptors; C009042:pristane