2009
DOI: 10.1186/1471-2180-9-194
|View full text |Cite
|
Sign up to set email alerts
|

Mycoplasma pneumoniae and/or Chlamydophila pneumoniae inoculation causing different aggravations in cholesterol-induced atherosclerosis in apoE KO male mice

Abstract: BackgroundChamydophila pneumoniae (CP) and/or Mycoplasma pneumoniae (MP) are two bacteria detected in vulnerable atheromas. In this study we aimed to analyze whether CP and/or MP aggravates atherosclerosis induced by cholesterol-enriched diet in C57BL/6 apoE KO male mice. Thirty male apoE KO mice aged eight weeks fed by a diet containing 1% cholesterol until 32 weeks of age were divided into four groups: the first was inoculated with CP (n = 7), the second with MP (n = 12), the third with both CP + MP (n = 5),… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

0
8
0
1

Year Published

2012
2012
2023
2023

Publication Types

Select...
8
1

Relationship

0
9

Authors

Journals

citations
Cited by 17 publications
(9 citation statements)
references
References 32 publications
0
8
0
1
Order By: Relevance
“…In vitro , the infection cycle in monocytes/macrophages typically last up to 3 days during which the bacterium triggers the upregulation of a number of genes linked to the development of atherosclerosis, secretion of a plethora of inflammatory cytokines, and increase the expression of endothelial adhesion molecules 15 16 . In addition, infection also alters cholesterol homeostasis 17 , activation of LDL receptor 18 , and induce atherosclerosis in apo-E KO mice 19 . Taken together, these observations suggest that the changes in the physiology of the host cell due to C. pneumoniae infection may contribute to the development of atherosclerosis.…”
mentioning
confidence: 99%
“…In vitro , the infection cycle in monocytes/macrophages typically last up to 3 days during which the bacterium triggers the upregulation of a number of genes linked to the development of atherosclerosis, secretion of a plethora of inflammatory cytokines, and increase the expression of endothelial adhesion molecules 15 16 . In addition, infection also alters cholesterol homeostasis 17 , activation of LDL receptor 18 , and induce atherosclerosis in apo-E KO mice 19 . Taken together, these observations suggest that the changes in the physiology of the host cell due to C. pneumoniae infection may contribute to the development of atherosclerosis.…”
mentioning
confidence: 99%
“…Also clinical studies have shown increased seropositivity to both Mp and Cp [10,11]. Inoculation of Cp and Mp in ApoE KO mice fed with cholesterol enriched diet caused aggravation of the size atherosclerotic plaques, inflammation or vessel remodeling [12]. In a recent work, we found higher amounts of both Cp and Mp in the adventitia of AAA than in severe aortic non-dilated atherosclerosis [13].…”
Section: Introductionmentioning
confidence: 93%
“…Experimental atherosclerotic plaques are produced in chickens by Marek's disease herpesvirus (Fabricant et al, 1978 ). C. pneumoniae and M. pneumoniae cause exacerbation of arterial plaques in hypercholesterolemic mice (Damy et al, 2009 ), and C. pneumoniae and influenza virus cause exacerbation of arterial plaques in mini-pigs with hypercholesterolemia (Birck et al, 2011 ).…”
Section: Infections and The Pathogenesis Of Atherosclerosismentioning
confidence: 99%