肺炎衣原体感染对C57BL/6J小鼠动脉粥样硬化形成的影响

目的:研究肺炎衣原体(CP)感染对C57BL/6J小鼠动脉粥样硬化(AS)形成的影响。方法:48只8周龄雄性C57BL/6J小鼠分为感染-高脂组、高脂组和感染组和对照组,喂养40周,取主动脉根部标本分析AS斑块面积,采用直接免疫荧光法检查血管壁CP抗原,微量免疫荧光法(Micro-IFA)检测CP特异性抗体IgG。结果:感染-高脂组小鼠平均AS斑块面积较高脂组增大[(135249±43748)μm2∶(96378±30945)μm2,P<0·05],感染组和对照组小鼠无AS样斑块形成。结论:CP感染可加速高脂饮食C57BL/6J小鼠的主动脉AS发展。     

肺炎衣原体感染对高脂血症小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、P50和c-Fos表达的影响

目的探讨肺炎衣原体感染对高脂血症小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、核因子κB和激活蛋白1表达的影响。方法48只C57BL/6J雌性小鼠分成对照组、感染组、高脂组和感染高脂组。14周后,通过间接免疫荧光标记法检测主动脉内皮细胞过氧化体增殖物激活型受体γ、P50(核因子κB亚单位)和c-Fos(激活蛋白1亚单位)表达情况。用苏丹Ⅳ对主动脉窦冰冻切片进行脂染色以检测主动脉窦动脉粥样硬化病灶情况并进行评分。结果主动脉窦动脉粥样硬化病灶评分在对照组和感染组无升高,而在高脂组和感染高脂组显著升高(P<0.01),且感染高脂组和高脂组相比差异有显著性(P<0.01)。和对照组相比,感染组、高脂组和感染高脂组小鼠主动脉内皮细胞过氧化体增殖物激活型受体γ、P50和c-Fos的表达是升高的,而在感染组、高脂组和感染高脂组3组之间过氧化体增殖物激活型受体γ、P50和c-Fos的表达差异无显著性。结论在肺炎衣原体感染和高脂血症的早期,小鼠主动脉内皮细胞的炎症通路已经激活。单独肺炎衣原体感染不能引起动脉粥样硬化的形成,但肺炎衣原体感染能加速高脂饮食引起的动脉粥样硬化形成。     

衣原体感染

沙眼衣原体和解脲支原体感染与输卵管性不孕症关系的研究，不孕和生育不良结局与妇女沙眼衣原体感染，肺炎衣原体感染对C57BL／6J小鼠动脉粥样硬化形成的影响。[编按]     

衣原体感染

肺炎衣原体感染致C57BL／6J小鼠内皮功能异常；肺炎衣原体感染和高脂血症对心肌细胞NF-kappa B和AP-1的影响；956例阴道分泌物标本沙眼衣原体检测结果分析；沙眼衣原体感染输血传播病毒感染状况调查；三种沙眼衣原体检测方法的对比评价.     

高脂、蛋氨酸饮食及CPn感染对小鼠动脉粥样硬化的影响

目的:探讨高脂饮食、高同型半胱氨酸血症及肺炎衣原体感染对小鼠血清IL-1β、Hs-CRP、内膜下单核细胞浸润计数、热休克蛋白染色表达的影响。方法:采用高脂及蛋氨酸饲料饲喂C57BL/6J小鼠并予以肺炎衣原体滴鼻感染(每隔周接种1次,共3次,6周时间)的方式造成AS模型。测定血清学及病理染色指标。结果:高脂+CPn感染和/或高同型半胱氨酸血症对小鼠的血清IL-1β、Hs-CRP、内膜下单核细胞浸润计数、热休克蛋白染色表达均有不同程度升高。结论:CPn感染、高同型半胱氨酸血症可增强高脂饮食致动脉粥样硬化的作用。     

丙丁酚可干预小鼠动脉粥样硬化病变并调节B类I型清道夫受体的表达

目的研究丙丁酚对高脂高胆固醇饲养的载脂蛋白E基因敲除小鼠和C57BL6/J小鼠血脂及动脉粥样硬化病变的影响,以及肝脏B类I型清道夫受体和PPARγ表达的变化。方法分别随机将20只载脂蛋白E-/-小鼠和20只C57BL6/J小鼠分为载脂蛋白E-/-高脂组和载脂蛋白E-/-高脂 0.5%丙丁酚组。动物喂     

丙丁酚可干预小鼠动脉粥样硬化病变并调节B类I型清道夫受体的表达

目的研究丙丁酚对高脂高胆固醇饲养的载脂蛋白E基因敲除小鼠和C57BL6／J小鼠血脂及动脉粥样硬化病变的影响，以及肝脏B类Ⅰ型清道夫受体和PPARγ表达的变化。方法分别随机将20只载脂蛋白E^-/^-小鼠和20只C57BL6／J小鼠分为载脂蛋白E^-／^-高脂组和载脂蛋白E^-/^-高脂＋0．5％丙丁酚组。     

动脉粥样硬化斑块内FIZZ1表达促进平滑肌细胞清道夫受体-A上调

目的探讨ApoE基因敲除鼠动脉粥样硬化斑块内FIZZ1表达情况及其对平滑肌细胞清道夫受体A(SR-A)表达的影响.方法C57BL/6J ApoE基因敲除鼠及C57BL/6J野生型小鼠各9只,分别喂养高脂饲料及普通饲料,24周后处死小鼠,石蜡包埋血管后做连续切片,行HE染色及FIZZ1免疫组化.用氧化型低密度脂蛋白(ox-LDL)以及终浓度分别为3×10-6mmol/L、9×10-6mmol/L、2.7×10-5mmol/L的FIZZ1刺激培养的平滑肌细胞,激光共聚焦显微镜确认SR-A表达后,流式细胞术检测FIZZ1对ox-LDL诱导的平滑肌细胞SR-A表达的影响.结果ApoE基因敲除鼠高脂饲养24周后,主动脉根部明显形成动脉粥样硬化,可见FIZZ1在动脉粥样硬化斑块内明显表达,同龄野生型C57BL/6J鼠正常血管壁内,未见FIZZ1表达,重组FIZZ1能明显促进ox-LDL诱导的平滑肌细胞SR-A表达(与对照组比较,P<0.01).结论C57BL/6J野生型小鼠正常血管不表达FIZZ1,C57BL/6JApoE基因敲除鼠动脉粥样斑块表达FIZZ1,FIZZ1促进ox-LDL诱导的平滑肌细胞SR-A表达,提示FIZZ1可能在ApoE基因敲除鼠动脉粥样硬化进展中起一定的促进作用.     

巨细胞病毒感染加剧apoE基因敲除小鼠动脉粥样硬化

目的建立巨细胞病毒(MCMV)感染的动脉粥样硬化动物模型,观察CMV感染是否可促使动脉粥样硬化发生。方法apoE基因敲除的C57BL/6雌性小鼠,随机分为四组,根据不同处理分为对照组、高脂高胆固醇饮食组、注射MCMV组和联合高脂高胆固醇饮食并注射MCMV组,每组9只。分别于饲养8、12和16周时处死小鼠,分离主动脉,病理切片观察动脉粥样硬化改变。结果对照组8周开始有内膜增厚,炎症细胞浸润,至16周尚无明显斑块形成;CMV感染组各阶段的炎症细胞浸润及泡沫细胞形成均比对照组和高脂饮食组严重,16周有明显的粥样斑块形成。而CMV感染合并高脂饮食组的病变最为严重。结论MCMV感染ApoE-KO小鼠可导致动脉粥样硬化的发生,高脂饮食与CMV感染对促动脉粥样硬化有协同作用。     

肺炎衣原体感染与冠心病的相关性研究

目的通过测定血清肺炎衣原体(TWAR)IgG、IgM抗体滴度水平,探讨肺炎衣原体感染与冠心病的相关性.方法应用间接微量免疫荧光法,测定115例冠心病病人(冠心病组)和60例健康人(正常对照组)血清肺炎衣原体IgC、IgM抗体滴度.结果冠心病组病人血清肺炎衣原体IgG平均几何滴度(GMT)(157.77±4.42)与正常对照组(119.93±4.29)相比有非常显著性差异(P<0.001).冠心病组肺炎衣原体既往感染阳性率明显高于正常对照组(70.4%vs36.7%,P<0.001),2组急性感染阳性率无明显差异(P>0.05).随着肺炎衣原体IgG抗体水平(IgG≥116)的增高,发生冠心病风险相对增高(OR4.36,95%CI 2.32～8.16).不稳定性心绞痛病人、急性心肌梗塞病人血清肺炎衣原体IgG平均几何滴度及感染阳性率均无明显差别,但两者与正常对照组相比均有非常显著性差异(P<0.001).结论研究结果表明,冠心病组病人肺炎衣原体感染率及血清肺炎衣原体IgG平均几何滴度均较高,有抗体者(IgG≥116)发生冠心病的风险相对增加,肺炎衣原体感染可能是构成冠心病发生发展的一个危险因子.     

Chlamydia pneumoniae infection accelerates hyperlipidemia induced atherosclerotic lesion development in C57BL/6J mice

Considerable evidence of an association between Chlamydia pneumoniae infections and cardiovascular disease has emerged. Animal models using genetically altered mice and hypercholesterolemic rabbits have shown a pathogenic role of C. pneumoniae in accelerating atherosclerotic plaque development. In the present study, we evaluated the effect of chronic C. pneumoniae infection on atherosclerosis in C57BL/6J mice, fed either a regular chow diet or a high fat, high cholesterol diet. Infected animals on an atherogenic diet developed significantly larger lesion areas compared with control mice at 18 weeks (2.5-fold increase; 4177+/-777 vs. 1650+/-808 microm(2); P<0.05) and 24 weeks of age (3.3-fold increase; 14139+/-4147 vs. 4298+/-869 microm(2); P<0.02). This study shows that chronic C. pneumoniae infection accelerates atherosclerotic lesion development in diet induced hypercholesterolemic mice, indicating that C. pneumoniae is a co-risk factor of hyperlipidemia in atherogenesis.     

Chlamydia pneumoniae does not increase atherosclerosis in the aortic root of apolipoprotein E-deficient mice

In epidemiological studies, an association between cardiovascular disease and Chlamydia pneumoniae (C pneumoniae) infection has been observed. Although C pneumoniae has been shown to be present in atherosclerotic lesions, a causal relationship between C pneumoniae infection and atherosclerosis has not been demonstrated. To study this question, we used 2 strains of apolipoprotein (apo) E-deficient mice. Eight-week-old mice on an FVB background that were maintained on either a low- or a high-fat diet were infected 3 times at 1-week intervals with C pneumoniae, and atherosclerotic lesions were measured in the aortic root at 10 weeks after the primary infection. In each of the diet groups, no difference in the extent of atherosclerosis could be observed between the C pneumoniae-infected and control animals. In further studies, 2 strains of apoE-deficient mice (FVB or C57BL/6J background) were infected 4 times at 3- to 4-week intervals, and the extent of atherosclerosis was analyzed 18 weeks later. The mice were kept on either a low- or a high-fat diet. The high-fat diet increased atherosclerosis, and a difference in atherosclerosis susceptibility between the mouse strains was observed. However, C pneumoniae infection did not influence lesion size in either mouse strain. On the other hand, C pneumoniae could not be demonstrated by polymerase chain reaction in any of the atherosclerotic lesions of the infected animals studied. A small decrease in serum cholesterol and triglyceride levels 3 days after the primary infection occurred, but after that no differences in serum lipid levels compared with those in noninfected animals were evident. In the myocardium of C pneumoniae-infected mice, no inflammatory signs could be observed. We conclude that under the experimental conditions used, C pneumoniae infection does not accelerate atherogenic changes in the aortic root of apoE-deficient mice.     

Effect of Chlamydia pneumoniae infection and hyperlipidaemia on the expression of PPARgamma, P50 and c-Fos in aortic endothelial cells in C57bL/6J mice

OBJECTIVE: To investigate the effect of C. pneumoniae infection and/or hyperlipidaemia on the expression of peroxisome proliferator-activated receptor gamma (PPARgamma), nuclear factor-kappa B (NF-kappaB) and activated protein-1 (AP-1) in aortic endothelial cells in C57BL/6J mice. METHODS AND RESULTS: Forty-eight, 8-week-old female C57BL/6J mice were divided into four groups:A, B, C and D (each twelve mice). Group A (as blank control) and B were fed a regular diet. Group C and D were fed an atherogenic diet (consisting of 15% fat, 2.5% cholesterol and 0.5% sodium cholate). Group B and D were infected with C. pneumoniae. Fourteen weeks later, the expression of PPARgamma, P50 (subunit of NF-kappaB) and c-Fos (subunit of AP-1) was determined by indirect immunofluorescence in the aortic endothelial cells. Slides of aortic sinus were prepared by cryosection, and stained with Sudan IV for examination of atherosclerotic plaque.The score of atherosclerotic plaque was determined by microscopy. The score of atherosclerotic plaque in group B was not increased, while it was significantly higher in groups C and D (P < 0.01), still the score in group D was higher than in group C (P < 0.01).The expression of PPARgamma, NF-kappaB and AP-1 in endothelial cells in aortic sinus was upregulated in group B, C and D, in comparison with group A (P < 0.05). There was no significant difference among groups B, C and D. CONCLUSION: The expression of PPARgamma, NF-kappaB and AP-1 was upregulated in the endothelial cells in mice infected with C. pneumoniae and/or fed with an atherogenic diet. An atherogenic diet or this diet combined with C. pneumoniae infection accelerated the process of atherosclerosis. The diet infected with C. pneumoniae alone would not accelerate this process. PPARgamma might play an anti-atherosclerotic role in this process.     

Mouse models of C. pneumoniae infection and atherosclerosis

Mouse models were used to determine whether Chlamydia pneumoniae establishes chronic infection of the aorta and contributes to atherogenesis. Persistent infection of the aorta occurred in 11 of 31 hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) mice but not in C57BL/6J mice fed a normal diet after a single inoculation and in both models following repeated inoculation with C. pneumoniae. Repeated inoculation of C57BL/6J mice resulted in inflammatory changes in the heart and aorta in 8 of 40 of mice; however, no atherosclerotic lesion development was observed. Repeated inoculation of apoE(-/-) mice resulted in a statistically significant increase in lesion area (n=43; P=.05). Although Chlamydia trachomatis disseminated to the aorta, persistent infection was not established and no statistically significant increase in lesion area occurred. These studies suggest that persistent infection of the aorta can lead to inflammatory changes in the absence of hyperlipidemia and accelerate lesion progress in concert with hyperlipidemia.     

Blocking very late antigen-4 integrin decreases leukocyte entry and fatty streak formation in mice fed an atherogenic diet

Atherosclerotic lesion development is characterized by the recruitment of leukocytes, principally monocytes, to the vessel wall. Considerable interest has been focused on the adhesion molecule(s) involved in leukocyte/endothelial interactions. The goal of the present study was to determine the role of the very late antigen-4 (VLA-4) integrin/ligand interaction in fatty streak development using murine models. Because alpha4 null mice are not viable, a peptidomimetic was used to block VLA-4-mediated leukocyte binding. The ability of a synthetic peptidomimetic of connecting segment-1 (CS-1 peptide) to block the recruitment of leukocytes and the accumulation of lipid in the aortic sinus of either wild-type mice (strain C57BL/6J) or mice with a low-density lipoprotein null mutation (LDLR-/-) maintained on an atherogenic diet was assessed. The active (Ac) CS-1 peptide or scrambled (Sc) CS-1 peptide was delivered subcutaneously into mice using a mini osmotic pump. Mice were exposed to the peptide for 24 to 36 hours before the onset of the atherogenic diet. In C57BL/6J mice, leukocyte entry into the aortic sinus, as assessed by en face preparations, was inhibited by the active peptide (Ac=28+/-4, Sc=54+/-6 monocytes/valve; P=0.004). Additionally, frozen sections stained with Oil Red O were analyzed to assess lipid accumulation in the aortic sinus. C57BL/6J mice that received the (Ac) compound demonstrated significantly reduced lesion areas as compared with mice that received the (Sc) peptide (Ac=4887+/-4438 microm2, Sc=15 009 +/-5619 microm2; P<0.0001). In a separate study, LDLR-/- mice were implanted with pumps containing either the (Ac) or (Sc) peptide before initiation of the atherogenic diet. Because LDLR-/- mice fed a chow diet displayed small lesions at 14 weeks, the effects of the peptide seen in these animals represented a change in early lipid accumulation rather than initiation. By using whole-mount preparations, the (Ac) but not the (Sc) peptide significantly reduced the area of lipid accumulation in the aortic sinus, resulting in an approximate 66% decrease. Plasma analysis from all studies revealed concentrations of peptide to be present at levels previously determined by in vitro analysis to block adhesion. (Ac) CS-1 peptide, which blocks VLA-4 on the leukocyte surface, is effective in reducing leukocyte recruitment and lipid accumulation in the aortic sinus. The present study provides in vivo evidence that the VLA-4 integrin plays an important role in the initiation of the atherosclerotic lesion and lipid accumulation, and it suggests a potential therapeutic strategy for this disease.     

Chlamydia pneumoniae infection and hyperlipidaemia-induced expression of P50 and c-Fos in the heart of C57BL6J mice

OBJECTIVE: The objective of this study was to investigate infection by Chlamydia pneumoniae (C. pneumoniae) and the combined effects of an atherogenic diet on the expression of AP-1 or the subunit of AP-1 (c-Fos) and NF-kappaB or the subunit of NF-kappaB (P50) in myocardial cells of C57BL/6J mice. METHODS AND RESULTS: Thirty-six 8-week-old female C57BL/6J mice were divided into three groups: A, B and C (twelve mice in each group). Mice in group A were fed an atherogenic diet (consisting of 15% fat and 2.5% cholesterol). Those in group B and C (as blank control) were fed a regular diet. The mice in group B were infected with C. pneumoniae. Fourteen weeks later, the expression of P50 (subunit of NF-kappaB) and c-Fos (subunit of AP-1) in the heart was determined by indirect immunofluorescence in the myocardial cells. Binding activity of NF-kappaB and AP-1 in the heart was determined by electrophoretic mobility shift assay (EMSA). The expression of NF-kappaB and AP-1 in the myocardial cells was upregulated in group A and B, compared with group C (P < 0.05). There was no significant difference between group A and B. CONCLUSION: The inflammatory process was already initiated in the myocardial cells in C57BL/6J mice at the early stage of C. pneumoniae infection and hyperlipidaemia. The expression of NF-kappaB and AP-1 was upregulated in mice infected by C. pneumoniae or fed an atherogenic diet. C. pneumoniae or hyperlipidaemia may involve the pathogenesis and progression of ischaemic cardiomyopathy.     

Exclusive expression of transmembrane TNF-alpha in mice reduces the inflammatory response in early lipid lesions of aortic sinus

We investigated the effect of transmembrane form of tumor necrosis factor-alpha (TNF) on atherosclerosis in mice. We compared the development of early atherosclerotic lesions in the aortic sinus of (1) TNF-deficient mice that express only a non-cleavable transmembrane form of TNF (tmTNF), (2) wild-type (WT) C57BL/6 mice, and (3) TNF-deficient mice (TNF(-/-)). All mice were fed an atherogenic diet for 20 weeks. Lipid deposition was the most prominent in WT mice (25030 +/- 5693 microm2), tended to be lower in tmTNF mice (13640+/- 2190 microm2, P > 0.05 versus WT mice) and rare in TNF(-/-) mice (1408 +/- 513 microm2, P < 0.05 versus tmTNF and P < 0.01 versus WT). Macrophage accumulation was five-fold lower (P < 0.05) in tmTNF than in WT mice. In addition, the alpha-actin immuno-reactivity of medial smooth muscle cells remained intact in tmTNF mice but not in WT mice. In WT mice, the plasma lipid profile was significantly more atherogenic than that of TNF(-/-) mice (P < 0.05), but not significantly different from that of tmTNF mice (P > 0.05). These results indicated that in contrast to TNF(-/-) mice, mice expressing exclusively tmTNF were not completely protected from early atherosclerotic lesion formation, although their lesions have a less inflammatory state than those of WT mice, which underlines the stronger proinflammatory potential of soluble TNF.     

Effect of aging on fatty streak formation in a diet-induced mouse model of atherosclerosis

Age is considered to be a major risk factor for atherosclerosis, but it is unclear whether age has a direct effect on susceptibility to atherosclerosis. Wild-type mice develop fatty streak lesions in the aortic root only when fed a cholate-containing high fat/cholesterol diet. To investigate the influence of age on fatty streak formation, young (10 weeks) and old (53 weeks) female C57BL/6 mice were fed an atherogenic diet containing 15% fat, 1.25% cholesterol and 0.5% sodium cholate for 12 weeks. Atherosclerotic lesions at the aortic root were measured after cryosections were stained with oil red O. Results showed that old mice developed a comparable size of aortic lesions with young counterparts (5,600 +/- 2,480 vs. 6,457 +/- 1,537 microm2/section; p = 0.77), although old mice had significantly higher plasma cholesterol levels than young mice on the atherogenic diet (p < 0.05). Plasma levels of soluble vascular cell adhesion molecule 1 were significantly higher in old mice than in young mice on both chow and Western diets (p < 0.005). These data indicate that age has no direct effect on atherosclerosis susceptibility although it is accompanied by elevations in plasma cholesterol and vascular cell adhesion molecule 1 levels in C57BL/6 mice. Thus, increased cardiovascular events with age are probably related to a progressive increase in plaque size rather than to an increase in atherosclerosis susceptibility.     

3-deazaadenosine prevents adhesion molecule expression and atherosclerotic lesion formation in the aortas of C57BL/6J mice

Adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) play an important role during the development of atherosclerosis. 3-Deazaadenosine (c(3)Ado), an adenosine analogue, inhibits endothelial-leukocyte adhesion and ICAM-1-expression in vitro. We hypothesized that c(3)Ado is able to prevent the expression of adhesion molecules and atherosclerotic lesion formation in female C57BL/6J mice. The animals were placed on an atherogenic diet with or without c(3)Ado for 9 weeks. Frozen cross sections of the proximal ascending aorta just beyond the aortic sinus were stained with oil red O, hematoxylin, and elastic van Gieson's stains and were analyzed by computer-aided planimetry for fatty plaque formation and neointimal proliferation. Monoclonal antibodies against CD11b (macrophages), VCAM-1, and ICAM-1 were used for immunohistochemistry. Mice on the atherogenic diet demonstrated multiple (5.4+/-1.6 per animal) lesions covering 3.4+/-2.8% of the endothelium and a marked neointima when compared with control mice (4501+/-775 versus 160+/-38 microm(2), P<0.001). Mice on the cholesterol-rich diet without c(3)Ado showed strong endothelial coexpression of ICAM-1 and VCAM-1. Moreover, there was a 10-fold increase in monocyte accumulation on the endothelial surface (33. 3+/-4.9 versus 3.8+/-1.2, P<0.004). In contrast, in mice treated with c(3)Ado, expression of ICAM-1 and VCAM-1 as well as monocyte adhesion and infiltration were almost completely inhibited. Furthermore, these mice did not show any fatty streak formation or neointima formation (125+/-32 microm(2)). Our results demonstrate that c(3)Ado can inhibit diet-induced fatty streak formation and the expression of endothelial ICAM-1 and VCAM-1 in C57BL/6J mice. This may provide a novel pharmacological approach in the prevention and treatment of atherosclerosis.     

C3H apoE(-/-) mice have less atherosclerosis than C57BL apoE(-/-) mice despite having a more atherogenic serum lipid profile

Wild-type C57BL mice are known to be susceptible to diet-induced atherosclerosis, whilst C3H mice are resistant. We investigated the effect of these background strains on the hyperlipidaemia and atherosclerosis that develops in mice deficient in apolipoprotein E (apoE(-/-)). Male and female apoE(-/-) mice on C3H/HeNHsd (C3H) and C57BL/6J (C57) backgrounds were fed atherogenic Western diet for 12 weeks. Serum cholesterol and triglyceride concentrations were measured and atherosclerosis quantified in the aortic sinus. C3H apoE(-/-) mice fed normal diet had 1.5 2 fold higher serum cholesterol levels than C57 apoE(-/-) mice and 4-5 fold higher serum triglyceride concentrations. Feeding Western diet caused a 4-5 fold increase in serum cholesterol in all mice, but levels of triglyceride were either attenuated or were unaffected in C3H apoE(-/-) and C57 apoE(-/-) mice, respectively. C3H apoE(-/-) mice had approximately 2 fold higher serum cholesterol and 4 fold higher triglyceride concentrations than the C57 apoE(-/-) mice throughout the study. Serum triglyceride concentrations were 35-108% higher in male C3H apoE(-/-) than female C3H apoE(-/-) mice. Most of the lipids were present in the very low density lipoprotein (VLDL)/chylomicron fraction in both strains of mice whether they were fed normal or Western diet. Notwithstanding the lower plasma lipid concentrations, atherosclerotic lesion areas were more than 2-fold larger in C57 apoE(-/-) than in C3H apoE(-/-) mice (males 68 +/- 11 x 10(3) vs 30 +/- 6 x 10(3) females 102 +/- 12 x 10(3) vs 41 +/- 8 x 10(3) microm2. mean +/- SEM).