Periodontal ligament and gingival fibroblasts from periodontitis patients are more active in interaction with Porphyromonas gingivalis

被引:63
作者
Scheres, N. [3 ,4 ]
Laine, M. L. [1 ,2 ]
Sipos, P. M. [5 ]
Bosch-Tijhof, C. J. [3 ]
Crielaard, W. [3 ]
de Vries, T. J. [1 ,2 ]
Everts, V. [4 ]
机构
[1] Univ Amsterdam, Dept Periodontol, ACTA, NL-1081 LA Amsterdam, Netherlands
[2] Vrije Univ Amsterdam, NL-1081 LA Amsterdam, Netherlands
[3] Univ Amsterdam, Dept Oral Microbiol, ACTA, NL-1081 LA Amsterdam, Netherlands
[4] Univ Amsterdam, Dept Oral Cell Biol, Res Inst MOVE, ACTA, NL-1081 LA Amsterdam, Netherlands
[5] Ctr Implantol & Periodontol Amstelveen, Amstelveen, Netherlands
关键词
inflammatory response; gene expression; Toll-like receptor; proinflammatory cytokine; TOLL-LIKE RECEPTORS; MHC GENE IKBL; PERIODONTOPATHOGENIC BACTERIA; CYTOKINE PRODUCTION; IMMUNE-RESPONSE; KAPPA-B; LIPOPOLYSACCHARIDE; ACTIVATION; HETEROGENEITY; INFLAMMATION;
D O I
10.1111/j.1600-0765.2011.01353.x
中图分类号
R78 [口腔科学];
学科分类号
100302 [口腔临床医学];
摘要
Background and Objective: Inflammatory responses of host cells to oral pathogenic bacteria, such as Porphyromonas gingivalis, are crucial in the development of periodontitis. Host cells, such as periodontal ligament and gingival fibroblasts, from periodontitis patients may respond to P. gingivalis in a different manner compared with cells from healthy persons. The aim of this study was to investigate inflammatory responses to viable P. gingivalis by periodontal ligament and gingival fibroblasts from periodontitis patients and healthy control subjects. Material and Methods: Primary periodontal ligament and gingival fibroblasts from periodontitis patients (n = 14) and healthy control subjects (n = 8) were challenged in vitro with viable P. gingivalis. Gene expression of Toll-like receptors (TLRs) 1, 2, 4, 6, 7 and 9, CD14, nuclear factor-kappa B1 and its putative inhibitor NF-kappa B inhibitor-like protein 1, and of interleukin-1 beta, interleukin-6, interleukin-8, tumour necrosis factor-alpha, monocyte chemotactic protein-1 and regulated upon activation, normal T-cel expressed, and secreted, were assessed by real-time PCR. Results: Periodontal ligament fibroblasts from periodontitis patients had a higher mRNA expression of TLR1, TLR4, TLR7 and CD14, and a lower expression of NFKBIL1, both before and after P. gingivalis challenge. In contrast, gingival fibroblasts from periodontitis patients had stronger induction of TLR1, TLR2 and TLR7 by P. gingivalis. Cytokine responses were not different between patients and control subjects. Interestingly, periodontal ligament, but not gingival, fibroblasts from P. gingivalis culture-positive persons responded more strongly to P. gingivalis than periodontal ligament fibroblasts from P. gingivalis-negative persons. Conclusion: Periodontal ligament and gingival fibroblasts respond to P. gingivalis in a different manner and may play different roles in periodontitis. Both subsets of fibroblasts from patients appear more active in interaction with P. gingivalis. Moreover, periodontal ligament fibroblasts from P. gingivalis-positive donors are more responsive to an in vitro P. gingivalis challenge.
引用
收藏
页码:407 / 416
页数:10
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