Journal of Microbiology

Research Support, Non-U.S. Gov'ts

Berberine Inhibits HEp-2 Cell Invasion Induced by Chlamydophila pneumoniae Infection: Li Jun Zhang , Li Jun Zhang , Wei Quan , Bei Bei Wang , Bing Ling Shen , Teng Teng Zhang , Yi Kang; J. Microbiol. 2011;49(5):834-840. Published online November 9, 2011; DOI: https://doi.org/10.1007/s12275-011-1051-z

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Abstract: This study investigated the inhibitory effects of berberine on Chlamydophila (Chlamydia) pneumoniae infection-induced HEp-2 cell invasion and explored the possible mechanisms involved in this process. C. pneumoniae infection resulted in a significant increase in HEp-2 cell invasion when compared with the control cells (P<0.01) in a Matrigel invasion assay. This enhanced cell invasion was strongly suppressed by berberine (50 μM) (P<0.01). In a cell adhesion assay, the infection-induced HEp-2 cell adhesion to Matrigel was also significantly inhibited by berberine (P<0.01). C. pneumoniae infection was found to promote HEp-2 cell migration remarkably (P<0.01), which was markedly suppressed by berberine (P<0.01) in the cell migration assays. There were no statistically significant differences in the expression of matrix metalloproteinase-1 (MMP-1) and MMP-9 in the infected cells and berberine did not change the expression of MMP-1 and MMP-9. These data suggest that berberine inhibits C. pneumoniae infection-induced HEp-2 cell invasion through suppressing HEp-2 cell adhesion and migration, but not through changing the expression of MMP-1 and MMP-9.

Detection of Enterovirus, Cytomegalovirus, and Chlamydia pneumoniae in Atheromas: Tae Won Kwon , Do Kyun Kim , Jeong Sook Ye , Won Joo Lee , Mi Sun Moon , Chul Hyun Joo , Heuiran Lee , Yoo Kyum Kim; J. Microbiol. 2004;42(4):299-304.

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Abstract: To investigate the presence of infectious agents in human atherosclerotic arterial tissues. Atherosclerotic plaques were removed from 128 patients undergoing carotid endarterectomy or other bypass procedures for occlusive disease, and from twenty normal arterial wall samples, obtained from transplant donors with no history of diabetes, hypertension, smoking, or hyperlipidemia. Using the polymerase chain reaction (PCR) or reverse transcription-PCR, these samples were analyzed for the presence of Chlamydia pneumoniae, cytomegalovirus, enterovirus, adenovirus, herpes simplex viruses types 1 and 2, and Epstein-Barr virus. The amplicons were then sequenced, and phylogenetic analyses were performed. Enteroviral RNA was found in 22 of 128 atherosclerotic vascular lesions (17.2%), and C. pneumoniae and cytomegalovirus were each found in 2 samples (1.6%). In contrast, adenovirus, herpes simplex viruses, and Epstein-Barr virus were not identified in any of the atherosclerotic samples. Enterovirus was detected in 6/24 (25.0%) aortas, 7/33 (21.2%) carotid arteries, 6/40 (15.0%) femoral arteries, and 3/31 (9.7%) radial arteries of patients with chronic renal failure. There were no infectious agents detected in any of the control specimens. Using phylogenetic analysis, the enterovirus isolates were clustered into 3 groups, arranged as echovirus 9 and coxsackieviruses B1 and B3. Enteroviral RNA was detected in 17.2% of atherosclerotic plaques, but was not observed in any of the control specimens. This suggests a connection between enteroviral infection and atherosclerosis. These findings differ from those of other studies, which found more frequent incidence of C. pneumoniae and cytomegalovirus infection in atherosclerotic plaques.

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