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Differential Induction of Human Beta‐Defensin Expression by Periodontal Commensals and Pathogens in Periodontal Pocket Epithelial Cells
Author(s) -
Vankeerberghen Anne,
Nuytten Hilde,
Dierickx Kurt,
Quirynen Marc,
Cassiman JeanJacques,
Cuppens Harry
Publication year - 2005
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2005.76.8.1293
Subject(s) - defensin , commensalism , beta defensin , microbiology and biotechnology , biology , medicine , immunology , bacteria , antimicrobial , genetics
Background: To investigate the possible role of beta‐defensins in gingival health and periodontal disease, we examined the effect of several stimuli on the expression of interleukin‐8 (IL‐8), human β‐defensin‐1, ‐2, ‐3, and ‐4 (hBD) in primary human diseased gingival epithelial (HGE) cell cultures from periodontitis patients by quantitative TaqMan reverse transcription polymerase chain reaction (RT‐PCR). Methods: Several strains of the periodontopathogens Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis were added to the cells, as well as the oral commensal bacteria Fusobacterium nucleatum and Escherichia coli . The induction by the proinflammatory stimuli phorbol 12‐myristate 13‐acetate (PMA) and tumor necrosis factor‐alpha (TNF‐α) was also tested. Results: In addition to the published observations (PMA induces hBD‐2 and ‐4; TNF‐α induces hBD‐2 and ‐3), it was found that PMA can upregulate hBD‐1 and hBD‐3, whereas TNF‐α can induce hBD‐4. The commensal bacteria were significant inducers of hBD‐2, hBD‐3, and IL‐8. The pathogen P. gingivalis induced hBD‐1 and hBD‐3 at different time points than the commensals, but no induction of IL‐8 and hBD‐2 could be observed. These data fit with the chemokine paralysis theory. A correlation was found between the pathogenicity of different serotypes of A. actinomycetemcomitans and the induction profiles of defensins and IL‐8. Conclusion: The results suggest that a correlation can be found in diseased oral epithelium between the defensin profiles that are induced and the pathogenicity of the oral bacterial strains. J Periodontol 2005;76:1293‐1303 .