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.


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.


CONCLUSIONS
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.
Huang
Bingsheng
B
Department of Cardiology, He Xian Memorial Hospital of Panyu District, Guangzhou, China. hbs8311@163.com
Dong
Yugang
Y
Cheng
Ying
Y
Xie
Qiang
Q
Lin
Guixiong
G
Wu
Yuyan
Y
Feng
Yanlin
Y
Li
Jingcao
J
Mai
Weiyi
W
D000818:Animals; D023521:Chlamydophila Infections / Q000235:genetics / Q000378:metabolism* / Q000382:microbiology; D016993:Chlamydophila pneumoniae / Q000302:isolation & purification; D004247:DNA / Q000235:genetics*; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D015870:Gene Expression; D006949:Hyperlipidemias / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000096:biosynthesis / Q000235:genetics*; D018808:Transcription Factor AP-1 / Q000096:biosynthesis / Q000235:genetics*
D016328:NF-kappa B; D018808:Transcription Factor AP-1; D004247:DNA