Berberine inhibits HEp-2 cell invasion induced by Chlamydophila pneumoniae infection.

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.

[Promoting effect of Chlamydia pneumoniae infection on human laryngeal carcinoma HEp-2 cell adhesion and migration].

OBJECTIVE: To explore the effect of Chlamydia pneumoniae (C.pn) infection on human laryngeal carcinoma cell line HEp-2 cell adhesion and migration, to further clarify the role and mechanism of C.pn infection in tumor metastasis. METHODS: HEp-2 cells were infected with C.pn after the culture and propagation of C.pn. The cytopathic effect was observed by microscopy. Morphological characteristics of C.pn inclusions in HEp-2 cells were examined by fluorescence microscopy and acridine orange staining. The ultrastructural changes of C.pn inclusions in the HEp-2 cells were examined by transmission electron microscopy (TEM). Cell adhesion assay was performed to investigate the effect of C.pn infection on the adhesion of HEp-2 cells to collagen I. Wound-healing assay and transwell assay were performed to explore the effect of C.pn infection on HEp-2 cell migration. RESULTS: At 72 h post-infection, C.pn infected-HEp-2 cells were swollen and partially desquamated. Numerous vacuoles (inclusions) were observed and C.pn inclusions occupied almost the whole cytoplasm of the HEp-2 cells. Grape-like C.pn inclusions were observed in the HEp-2 cells stained with acridine orange under a fluorescence microscope at 72 h after infection. Under TEM, there were more mature pear-shaped elementary bodies, but less larger and round reticulate bodies in the HEp-2 cells infected with C.pn for 72 h. In the cell adhesion assay, the A value in C.pn infection group was 0.669 ± 0.011, significantly higher than that in the control group (0.558 ± 0.005) at 2 h after infection (P < 0.001). The cell adhesion ratio in the C.pn infection group was 119.89%. The migration distance of C.pn infected-HEp-2 cells in the wound-healing assay was significantly longer than that of control cells at 24 h after infection (P < 0.05). HEp-2 cells infected with C.pn for 12 h migrated more than the control cells in the transwell assay (23.40 ± 2.41 vs 10.40 ± 1.67) (P < 0.001). CONCLUSIONS: C.pn infection can significantly promote HEp-2 cell adhesion to collagen I and migration of HEp-2 cells, indicating that C.pn infection may play an important role in promoting the metastasis of laryngeal cancer.