Impact of Fusobacterium Nucleatum and Porphyromonas Gingivalis Modulation on the Cell Cycle and Cytokines Production of KB Cells.

doi:10.13701/j.cnki.kqyxyj.2016.03.001

Abstract

Abstract: Objective: To investigate the effects of P. gingivalis/F. nucleatum on the cell cycle and cytokines production of KB cells.Methods: In vitro models were established with KB cells co-cultured with P. gingivalis/F. nucleatum either alone or in combination. Transmission electron microscopy was used to observed invasive ability, the change of cell cycle of KB cells was detected by flow cytometry, and the production of interleukin-6 (IL-6) and interleukin-8 (IL-8) was analyzed by enzyme-linked immunoadsordent assay. Results: Eight-hour co-infection with P. gingivalis/F. nucleatum slowed the cell cycle of KB cells, while eight-hour co-infection accelerated the cell cycle. The production of IL-6 and IL-8 was significantly up-regulated after co-infection with P. gingivalis/F. nucleatum in a time dependent and F. nucleatum density related manner. Conclusion: Combination of oral pathogens can stimulate tumorigenesis and inflammation response in OSCC.

Key words: Fusobacterium nucleatum , Porphyromonas gingivalis , Cytokines , Cell cycle, KB cells

CLC Number:

R781.4

WANG Qing-xuan, LIU Jun-chao, PAN Ya-ping. Impact of Fusobacterium Nucleatum and Porphyromonas Gingivalis Modulation on the Cell Cycle and Cytokines Production of KB Cells.[J]. Journal of Oral Science Research, 2016, 32(3): 211-215.

References

[1] Cutler CW, Kalmar JR, Genco CA. Pathogenic strategies of the oral anaerobe, Porphyromonas gingivalis [J]. Trends Microbiol, 1995, 3(2)∶45-51
[2] Kolenbrander PE. Multispecies communities:Interspecies interactions influence growth on saliva as sole nutritional source [J]. Int J Oral Sci, 2011, 3(2)∶49-54
[3] Petti S, Scully C. Oral cancer knowledge and awareness: primary and secondary effects of an information leaflet [J]. Oral Oncol, 2007, 43(4)∶408-415
[4] Nagy KN,Sonkodi I,Szoke I,et al.The microflora associated with human oral carcinomas [J]. Oral oncology, 1998, 34(4)∶304-308
[5] Sayehmiri F, Sayehmiri K, Asadollahi K, et al. The prevalence rate of Porphyromonas gingivalis and its association with cancer: A systematic review and meta-analysis [J]. Int J Immunopathol Pharmacol, 2015, 28(2)∶160-167
[6] Ha NH, Woo BH, Kim DJ, et al. Prolonged and repetitive exposure to Porphyromonas gingivalis increases aggressiveness of oral cancer cells by promoting acquisition of cancer stem cell properties [J]. Tumour Biol, 2015,36(12)∶9947-9960
[7] Binder Gallimidi A, Fischman S, Revach B, et al. Periodontal pathogens porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model [J]. Oncotarget, 2015, 6(26)∶22613-22623
[8] Metzger Z, Blasbalg J, Dotan M, et al. Enhanced attachment of Porphyromonas gingivalis to human firbroblasts mediated by Fusobacterium nucleatum [J]. J Endo, 2009, 35(1)∶82-85
[9] Saito A, Inagaki S, Kimizuka R, et al. Fusobacterium nucleatum enhances invasion of human gingival epithelial and aortic endothelial cells by Porphyromonas gingivalis [J]. FEMS Immunol Med Microbiol, 2008, 54(3)∶349-355
[10] Pan C, Xu X, Tan L, et al. The effects of Porphyromonas gingivalison the cell cycle progression of human gingival epithelial cells [J]. Oral Diseases, 2014, 20(1)∶100-108
[11] 潘春玲,赵海礁,谭丽思,等.牙龈卟啉单胞菌感染MG63细胞对细胞周期的影响[J].口腔医学研究,2015,31(9)∶863-866
[12] Bhattacharya R, Xu F, Dong G, et al. Effect of bacteria on the wound healing behavior of oral epithelial cells [J]. PLoS One, 2014, 9(2)∶e89475
[13] Shenker BJ, Datar S. Fusobacterium nucleatum inhibits human T-cell activation by arresting cells in the mid-G1 phase of the cell cycle [J]. Infect Immun, 1995, 63(12)∶4830-4836
[14] Binder Gallimidi A, Fischman S, Revach B, et al. Periodontal pathogens Porphyromonas gingivalis and Fusobacterium nucleatum promote tumor progression in an oral-specific chemical carcinogenesis model [J]. Oncotarget, 2015, 6(26)∶22613-22623
[15] Jian SL, Hsieh HY, Liao CT, et al. Gα12 Drives Invasion of Oral Squamous Cell Carcinoma through up-regulation of proinflammatory Cytokines [J]. PLoS One, 2013, 8(6)∶e66133
[16] 郭永华,吴亚菲, 刘天佳, 等. 不同fimA基因型牙龈卟啉单胞菌刺激口腔上皮细胞白细胞介素-8的表达[J].华西口腔医学杂志,2008,32(06)∶652-655
[17] Guentsch A, Ronnebeck M, Puklo M, et al. Influence of serum on interaction of Porphyromonas gingivalis ATCC 33277 and Aggregatibacter actinomycetemcomitans Y4 with an epithelial cell line [J]. J Periodontal Res, 2010, 45(2)∶229-238
[18] Yee M, Kim S, Sethi P, et al. Porphyromonas gingivalis stimulates IL-6 and IL-8 secretion in GMSM-K, HSC-3 and H413 oral epithelial cells [J]. Anaerobe., 2014, 28(1)∶62-67
[19] Watanabe K, Yilmaz O, Nakhjiri SF, et al. Association of mitogen-activated protein kinase pathways with gingival epithelial cell responses to Porphyromonas gingivalis infection [J]. Infect Immun, 2001, 69(11)∶6731-6737