Objective To investigate the recent studies about the relationship between Chlamydia pneumoniae and abdominal aortic aneurysm. Methods The current literatures about the relationship between Chlamydia pneumoniae and abdominal aortic aneurysm were reviewed. Results Chlamydia pneumoniae is one of the most important factors for the formation of abdominal aortic aneurysm since Chlamydia pneumoniae can cause abdominal aortic aneurysm through the metabolism of matrix metalloproteinases, the apoptosis of smooth muscle cells in the vessels and the chronic infection of the wall of the aneurysm. Conclusion There maybe a distinguishingly close relationship between Chlamydia pneumoniae and abdominal aortic aneurysm, and Chlamydia pneumoiae may take an important role in the development and progress of the abdominal aortic aneurysm.
Objective To investigate whether Chlamydia pneumoniae alters the expression of TLR2 mRNA and p38 MAPK mRNA in mice with Chlamydia pneumoniae infection in TLR2-p38 MAPK-dependent pathway, subsequently leading to the release of cytokines. Methods Seventy-two male C3H/HeJmice were randomly divided into three groups as follow: a normal control group, a C. pneumoniae-inoculated group, and a C. pneumoniae-inoculated with SB203580 treatment group. The mice in the three groups were sacrificed on 1st, 4th, 7th, 14th day separately, and lung tissues were sampled for measurement. The expression changes of TLR2 mRNA and p38 MAPK mRNA in the mice lung tissue were measured by semi-quantitative RT-PCR. The concentrations of TNF-αin the lung tissue were measured by ELISA.Results Compared with those in the normal group, the expressions of TLR2 mRNA and p38MAPK mRNA in the lung tissue increased quickly after C. pneumoniae infection, which was especially obvious on day 4 and on day 7, the expression level of TLR2 mRNA on day 7 was markedly higher than that of the normal group [ ( 7. 24 ±1. 78) mg/L vs.( 0. 64 ±0. 14) mg/L, P lt;0. 05] ; The expression level of p38 MAPK mRNA on day 4 was markedly higher than that of the normal group [ ( 9. 267 ±1. 813) mg/L vs. ( 3. 734 ±0. 946) mg/L, P lt;0. 05] . After 14 days, C. pneumoniae infection of mice was attenuated, the concentration of TNF-α in the lung tissue increased, and was clearly higher than that of the normal control group, peaking on day 4 [ ( 77. 29 ±9. 66) pg/mg] . Treatment with SB203580 could effectively inhibit TLR2 mRNA and p38 MAPK mRNA expression in lung, which was especially obvious on day 4 and on day 7. The expression level of TLR2 mRNA on day 7 was ( 0. 269 ±0. 09) mg/L, and the expression level of p38 MAPK mRNA on day 7 [ ( 0. 002 ±0. 001) mg/L] was even more obviously attenuated, the concentration of TNF-α in the lung tissue markedly decreased when compared with that in the infected group, and its concentration on day 4 [ ( 25. 76 ±3. 49) pg/mg] lowered more clearly. Conclusions The alteration of TLR2-p38 MAPKdependent signal pathway in lungs is closely connected with Chlamydia pneumoniae infection. SB203580 treatment can effectively controll the elevation of TLR2 mRNA and p38 MAPK mRNA expressions in lung. It can effectively control the TLR2-MAPK signal transduction pathway.
Objective To review the association between chlamydia pneumoniae (CP) infection and cerebral infarction. Methods We electronically searched MEDLINE, BIOSIS, VIP database, and China Full Text Journal Database from Jan. 1990 through Dec. 2007 to identify case-control studies about the association of CP and cerebral infarction. The quality of the included studies was assessed and the RevMan 4.2 software was used for meta-analyses. Results A total of 22 studies were included. The results of meta-analyses showed: ① When the microimmunofluorescence (MIF) method was used to examine CP antibody in serum, the positive rate of the cerebral infarction group was higher than that of the control group when the positive infection was defined by IgA≥1?16 [n=8, OR=2.18, 95%CI (1.49 to 3.49), Plt;0.0001]; but when positive infection was defined by IgA≥1?32 (n=3), IgG≥1?32 (n=6), or IgG≥1?64 (n=5), there were no significant differences in the positive rate between the two groups [OR (95%CI) were 1.47 (0.97 to 2.24), 1.24 (0.82 to 1.86), and 1.23 (0.98 to 1.55), respectively]; ② When the ELISA method was used to examine CP-IgG antibody in serum, the positive rate of the cerebral infarction group was higher than that of the controlled group [n=8, OR=2.40, 95%CI (1.42 to 4.06), P=0.000 2]. ③ The acute and chronic CP infections were associated with the incidence of cerebral infarction [n=4, OR=7.22, 95%CI (2.68 to 19.49); n=4, OR=4.30, 95%CI (3.40 to 7.40)]. Conclusion ① The association between CP infection and cerebral infarction is determined by the positive criterion. IgA antibody is more sensitive than the IgG antibody. When the positive infection is determined by IgA≥1?16, CP infection is associated with cerebral infarction. ② The results of ELISA for examining CP-IgG support the association between CP infection and cerebral infarction. ③ Both acute and chronic CP infections are associated with cerebral infarction, but these associations needed to be proven by more scientific studies.