Porphyromonas gingivalis stimulates IL-6 and IL-8 secretion in GMSM-K, HSC-3 and H413 oral epithelial cells

被引:39
作者
Yee, Michael [1 ]
Kim, Shawn [1 ]
Sethi, Pushpinder [1 ]
Duezguenes, Nejat [1 ]
Konopka, Krystyna [1 ]
机构
[1] Univ Pacific, Arthur A Dugoni Sch Dent, Dept Biomed Sci, San Francisco, CA 94115 USA
关键词
Porphyromonas gingivalis; Bacteria-cell interactions; Interleukin-6; Interleukin-8; Epithelial cells; Inflammatory response; PERIODONTAL-DISEASE; CYTOKINE PRODUCTION; GINGIPAINS; INTERLEUKIN-8; RESPONSES; MODULATION; BACTERIA; LINE; PATHOGENESIS; MECHANISMS;
D O I
10.1016/j.anaerobe.2014.05.011
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Infection of oral epithelial cells with periodontopathogenic bacteria results in the production of proinflammatory cytokines involved in the initiation and progression of periodontal disease. The purpose of this study was to examine the release of interleukin (IL)-6 and IL-8 by oral epithelial cells after exposure to Pozphyromonas gingivalis. Non-tumor-derived, immortalized human GMSM-K cells, and human oral squamous cell carcinoma, HSC-3 and H413 cells, were co-cultured with live and heat-inactivated P. gingivalis 2561 (ATCC 33277) and W83 (ATCC BAA-308 (TM)). IL-6 and IL-8 were quantified in the culture supernatants after 6 and 24 h. The basal levels of both cytokines and the responses to P. gingivalis were strongly dependent on cell type. GMSM-K cells produced less IL-8 than HSC-3 and H413 cells. Live P. gingivalis induced significant IL-6 and IL-8 secretion in GMSM-K and HSC-3 cells, and heat-inactivation of bacteria enhanced greatly IL-6 and IL-8 stimulation in these cells. Uninfected H413 cells produced high levels of IL-6 and IL-8, but were not responsive to live P. gingivalis; heat-inactivated P. gingivalis up-regulated IL-6 and IL-8 secretion in these cells. Since base-line secretion of IL-6 and IL-8, and responses to P. gingivalis depend on the cell type, conclusions on the responses to P. gingivalis should not be based on studies with a single cell type. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:62 / 67
页数:6
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