However, in apoE KO mice, the loss of

the ligand for lipi

However, in apoE KO mice, the loss of

the ligand for lipid particle receptors is associated with an increase in total cholesterol due to mainly LDL particle accumulation. Basal cholesterolemia of apoE KO mice is up to five times higher than that of animals of the same strain without the genetic defect, that aggravate with cholesterol enriched diet [31]. Development of atherosclerotic lesions is also affected by cholesterol reverse transport in which apoE plays a pivotal role. Salubrinal ic50 In our study, lower level of LDL was seen in infected groups, mainly in MP group. However, the statistical analysis was not performed because we analyzed a pool of sera from each group. Plaque rupture is not usually present in experimental atherosclerosis in animals including the apoE KO mice, which are considered an adequate experimental model for atherosclerosis studies [32]. In the present study it was not found ruptured

selleck chemicals llc plaques either. In humans, vulnerable plaques exhibited MCC950 research buy a third class of microbes, the Archaea [33], in close association with CP and MP. Conclusion Intraperitoneal inoculation of Chlamydia pneumoniae (CP), Mycoplasma pneumoniae (MP) or both microbes caused aggravation of experimental atherosclerosis induced by cholesterol-enriched diet, with different characteristics. MP or CP caused more extensive atherosclerotic lesions in the aorta, CP resulted in mafosfamide increased plaque height with positive vessel remodeling and co-inoculation of MP + CP led to the development of more obstructive lesions due to smaller plaques associated with no vessel remodeling. Methods Animals This study was approved by the Institutional Animal Welfare and Use Committee (Authorization number: SDS 2371/03/165). Animals were treated in accordance with the Guide for the Care and Use of Laboratory Animals [34]. Colonies of C57BL/6 apoE

KO mice were obtained from original animals of Jackson Laboratories (Bar Harbor, ME). The foundation colonies were maintained in a Trexler isolator (Veco do Brasil, Campinas). Pups weaned at 21-days of age were housed in microisolator cages, under biosafety level 2 conditions, with free access to sterile water and regular irradiated rations. The mice were serologically negative for murine cytomegalovirus (MCMV), mouse hepatitis virus (MHV), minute virus of mice (MVM), M. pulmonis, M. pneumoniae and C. pneumoniae. The mice were inoculated intraperitoneally with either 1 × 106 inclusion-forming units (IFU) of C. pneumoniae (CP), AR-39 (ATCC 53592), kindly provided by Prof. Mário Hirata of the Institute of Pharmaceutical Sciences of Sao Paulo University, and/or 1 × 106 colony forming units (CFU) of M. pneumoniae (MP) strain FH, (ATTC 15531), from the Institute of Biomedical Sciences of Sao Paulo University.

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