Mycoplasma genitalium lipid-associated membrane proteins induce human monocytic cell express proinflammatory cytokines and apoptosis by activating nuclear factor κB
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National Natural Science Foundation of China (30570093);Natural Science Foundation of Hunan Province (06JJ504)

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    Abstract:

    Designed to investigate the potential pathogenicity of Mycoplasma genitalium (M. genitalium) and its molecular mechanisms responsible for the induction of proinflammatory cytokines gene expression in human monocytic cells (THP-1) stimulated by lipid-associated membrane proteins (LAMPs) prepared from M. genitalium. THP-1 cells were stimulated with LAMPs to analyze the production of proinflammatory cytokines and the expression of mRNA was detected by RT-PCR. Cell apoptosis was detected in THP-1 cells by Annexin V-propidium iodide staining. The activity of transcriptional factors, NF-κB, was examined in THP-1 cells treated with LAMPs by EMSA. The effects of pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB, on the production of proinflammatory cytokines, the expression of mRNA and apoptosis were also examined in THP-1 cells treated with LAMPs. M.genitalium LAMPs stimulate THP-1 cells to produce TNF-α、IL-1β and IL-6 in dose- and time-dependent manner. The mRNA levels and cell apoptosis are also downregulated in response to LAMPs stimulation and inhibited by PDTC treatment. M.genitalium LAMPs are found to trigger NF-κB activation, a possible mechanism for the induction of mRNA expression and the cell apoptosis. This study demonstrated that M.genitalium may be an important etiological factor of certain disease due to the ability of LAMPs to stimulated the expression of mRNA and apoptosis, which is probably mediated through the activation of NF-κB.

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QIU Hong, WU Yi-mou, YOU Xiao-xing, YU Ming-jun, ZENG Yan-hua. Mycoplasma genitalium lipid-associated membrane proteins induce human monocytic cell express proinflammatory cytokines and apoptosis by activating nuclear factor κB. [J]. Acta Microbiologica Sinica, 2007, 47(5): 899-904

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  • Received:January 17,2007
  • Revised:July 09,2007
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