P. gingivalis accelerates gingival epithelial cell progression through the cell cycle

被引:145
作者
Kuboniwa, Masae [2 ]
Hasegawa, Yoshiaki [3 ]
Mao, Song [1 ]
Shizukuishi, Satoshi [2 ]
Amano, Atsuo [4 ]
Lamont, Richard J. [1 ]
Yilmaz, Oezlem [5 ,6 ]
机构
[1] Univ Florida, Coll Dent, Dept Oral Biol, Gainesville, FL 32610 USA
[2] Osaka Univ, Grad Sch Dent, Dept Prevent Dent, Osaka, Japan
[3] Aichi Gakuin Univ, Sch Dent, Dept Microbiol, Nagoya, Aichi 464, Japan
[4] Osaka Univ, Grad Sch Dent, Dept Oral Frontier Biol, Osaka, Japan
[5] Univ Florida, Dept Periodontol, Gainesville, FL 32610 USA
[6] Univ Florida, Shands Canc Ctr, Gainesville, FL 32610 USA
关键词
microbe-cell interactions; periodontal disease; cell proliferation;
D O I
10.1016/j.micinf.2007.10.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
P. gingivalis, an opportunistic pathogen in periodontal disease, can reside within the epithelial cells that line the gingival crevice. A proteomic analysis revealed that infection of gingival epithelial cells with P. gingivalis induces broadly based changes in the level and phosphorylation status of proteins that exert multi-level control on the eukaryotic cell cycle. Pathways that were impacted by P. gingivalis included those involving cyclins, p53 and PI3K. The predicted infection-dependent phenotype was confirmed by cytofluorimetry that showed an enhanced proliferation rate of gingival epithelial cells infected with P. gingivalis associated with accelerated progression through the S-phase. Elevated cell proliferation was dependent on the presence of the long fimbriae of P. gingivalis. The ability of P. gingivalis, a common inhabitant of the subgingival crevice, to accelerate cell cycling could have biological consequences for barrier and signaling functions, and for physiological status, of the gingival epithelium. (C) 2007 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:122 / 128
页数:7
相关论文
共 30 条
[1]   Fluorescence image analysis of the association between Porphyromonas gingivalis and gingival epithelial cells [J].
Belton, CM ;
Izutsu, KT ;
Goodwin, PC ;
Park, Y ;
Lamont, RJ .
CELLULAR MICROBIOLOGY, 1999, 1 (03) :215-223
[2]   Multiple levels of cyclin specificity in cell-cycle control [J].
Bloom, Joanna ;
Cross, Frederick R. .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2007, 8 (02) :149-160
[3]   Cyclins and cdks in development and cancer: a perspective [J].
Deshpande, A ;
Sicinski, P ;
Hinds, PW .
ONCOGENE, 2005, 24 (17) :2909-2915
[4]   5,6-carboxyfluorescein diacetate succinimidyl ester-labeled apoptotic and necrotic as well as detergent-treated cells can be traced in composite cell samples [J].
Dumitriu, IE ;
Mohr, WG ;
Kolowos, W ;
Kern, P ;
Kalden, JR ;
Herrmann, M .
ANALYTICAL BIOCHEMISTRY, 2001, 299 (02) :247-252
[5]   Host-pathogen interactions:: a diversity of themes, a variety of molecular machines [J].
Galán, JE ;
Cossart, P .
CURRENT OPINION IN MICROBIOLOGY, 2005, 8 (01) :1-3
[6]   Phosphoinositide 3-kinase controls early and late events in mammalian cell division [J].
García, Z ;
Kumar, A ;
Marqués, M ;
Cortés, I ;
Carrera, AC .
EMBO JOURNAL, 2006, 25 (04) :655-661
[7]   Microbial pathogenesis and cytoskeletal function [J].
Gruenheid, S ;
Finlay, BB .
NATURE, 2003, 422 (6933) :775-781
[8]   Distinct transcriptional profiles characterize oral epithelium-microbiota interactions [J].
Handfield, M ;
Mans, JJ ;
Zheng, GL ;
Lopez, MC ;
Mao, S ;
Progulske-Fox, A ;
Narasimhan, G ;
Baker, HV ;
Lamont, RJ .
CELLULAR MICROBIOLOGY, 2005, 7 (06) :811-823
[9]   Gingival epithelial cell transcriptional responses to commensal and opportunistic oral microbial species [J].
Hasegawa, Yoshiaki ;
Mans, Jeffrey J. ;
Mao, Song ;
Lopez, M. Cecilia ;
Baker, Henry V. ;
Handfield, Martin ;
Lamont, Richard J. .
INFECTION AND IMMUNITY, 2007, 75 (05) :2540-2547
[10]   Akt/PKB signaling mechanisms in cancer and chemoresistance [J].
Kim, D ;
Dan, HC ;
Park, S ;
Yang, L ;
Liu, QY ;
Kaneko, S ;
Ning, JY ;
He, LL ;
Yang, H ;
Sun, M ;
Nicosia, SV ;
Cheng, JQ .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2005, 10 :975-987