Correlation of Chlamydia pneumoniae infection with primary biliary cirrhosis
Hai-Ying Liu1, An-Mei Deng, Jian Zhang
1Clinical Laboratory, General Hospital of Guangzhou Military Command of PLA, Guangzhou 510010, Guangdong Province, China. xiangliuhaiying@21cn.com
Insights
Chlamydia pneumoniae (Cpn) infection is not a cause of primary biliary cirrhosis (PBC). However, Cpn infection may contribute to elevated IgM levels observed in PBC patients.
Area of Science:
- Hepatology
- Infectious Diseases
- Immunology
Background:
- Primary biliary cirrhosis (PBC) is a chronic liver disease of autoimmune origin.
- The role of infectious agents, such as Chlamydia pneumoniae (Cpn), in the pathogenesis of PBC remains unclear.
Purpose of the Study:
- To investigate the association between Chlamydia pneumoniae infection and primary biliary cirrhosis.
- To determine if Cpn infection is a triggering or causative agent in PBC.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to detect Cpn IgG and IgM antibodies.
- 41 PBC patients, 70 post-hepatitis cirrhosis patients, and 57 healthy controls were included.
- Seroprevalence and antibody levels of Cpn were compared across groups.
Main Results:
- Significantly higher Cpn IgG levels and seroprevalence were found in PBC and post-hepatitis cirrhosis groups compared to healthy controls.
- Elevated Cpn IgM seroprevalence was observed in PBC patients.
- Cpn IgM, but not Cpn IgG, correlated with high IgM concentrations in PBC patients.
Conclusions:
- Chlamydia pneumoniae infection is unlikely to be a causative agent of PBC.
- Cpn infection may contribute to the elevated IgM levels commonly seen in PBC patients.
Aim:
To evaluate the association between Chlamydia pneumoniae (Cpn) infection and primary biliary cirrhosis (PBC).
Methods:
Cpn IgG and IgM were determined by enzyme-linked immunosorbent assay (ELISA) in 41 well-established PBC patients and two race-matched control groups (post-hepatitis cirrhosis, n = 70; healthy controls, n = 57).
Results:
The mean level and seroprevalence of Cpn IgG in PBC group and post-hepatitis cirrhosis (PHC) group were significantly higher than those in healthy controls (46.8+/-43.4 RU/mL, 49.5+/-45.2 RU/mL vs 28.3+/-32.7 RU/mL; 68.3%, 71.4%, 42.1%, respectively; P<0.05). There was a remarkably elevated seroprevalence of Cpn IgM in patients with PBC (22.0%) compared to the PHC and healthy control (HC) groups. For the PBC patients versus the HCs, the odds ratios (ORs) of the presence of Cpn IgG and IgM were 2.7 (95% CI 0.9-6.1) and 5.1 (95% CI 1.4-18.5), respectively. Though there was no correlation in the level of Cpn IgG with total IgG in sera of patients with PBC (r = -0.857, P = 0.344>0.05), Cpn IgM was related with the abnormally high concentrations of total IgM in PBC group.
Conclusion:
The results of this study do not support the hypothesis that infection with Chlamydia pneumoniae may be a triggering agent or even a causative agent in PBC, but suggest that Chlamydia pneumoniae infection probably contributes to the high level of IgM present in most patients with PBC.
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