Effect of microphage infectivity potentiator of Chlamydia psittaci on the production of proinflammatory cytokines and apoptosis in host cells
ZENG Xin-dian1, ZHANG Wan-qi2, FU Xi-zong1, ZHOU Peng1, ZHOU Pu-fan1, TANG Ting1, CHEN Xi1, HU Chun-sheng3, CHEN Li-li1
1.School of Public Health, University of South China, Hengyang, Hunan 421001, China; 2.Chuanshan College, University of South China, Hengyang, Hunan 421001, China; 3.Hunan Provincial Center for Disease Control and Prevention, Changsha, Hunan 410005, China
Abstract:Objective To study the role of microphage infectivity potentiator (Mip) of Chlamydia psittaci (C. psittaci) on the production of proinflammatory cytokines in human acute monocytic leukemia cell line (THP-1) cells and apoptosis inhibition in HeLa cells. Methods Different concentration of recombinant Mip protein was used to stimulate THP-1 cells, and the expression of interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) was detected by enzyme-linked immunosorbent assay (ELISA). The number of apoptosis cells was tested by fluorescence staining and flow cytometry after HeLa cells were stimulated with recombinant Mip protein. ResultsC. psittaci Mip could stimulate THP-1 cells to produce IL-8 and TNF-α in a dose- and time-dependent manner. The levels of IL-8 and TNF-α in THP-1 cells treated with different concentration of recombinant Mip protein were significantly higher than those in phosphate buffer salinetreated groups (both P<0.05). The production of IL-8 (105.01 pg/ml) and TNF-α (50.52 pg/ml) reached the highest levels when the concentration of recombinant Mip protein was 16 μg/ml. The fluorescent Hoechst 32258 staining and flow cytometric assay showed that C. psittaci Mip protein could inhibit the apoptosis of staurosporine-treated HeLa cells to some extent, and the rate of apoptosis cells reduced 4.48% when the concentration of recombinant Mip protein was 20 μg/ml. ConclusionsC. psittaci Mip protein can stimulate THP-1 cells to produce IL-8 and TNF-α and inhibit HeLa cell apoptosis.
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