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Innate immune responses of gingival epithelial cells to nonperiodontopathic and periodontopathic bacteria

Cited 88 time in Web of Science Cited 92 time in Scopus
Authors

Ji, S.; Kim, Y.; Min, B.-M.; Han, S. H.; Choi, Y.

Issue Date
2007-12
Publisher
Blackwell Publishing Inc.
Citation
Journal of Periodontal Research, Vol.42 No.6, pp.503-510
Abstract
Background and Objective: We have previously reported different susceptibilities of periodontopathic and nonperiodontopathic bacteria to antimicrobial peptides and phagocytosis by neutrophils. Differences between the two groups of bacteria may exist also in their ability to induce immune responses from the host. Therefore, we evaluated the effects of various oral bacteria on innate immune responses by gingival epithelial cells. Material and Methods: HOK-16B cells were cocultured with live or lysed nonperiodontopathic (n = 3) and periodontopathic (n = 5) bacterial species. The levels of human beta defensin-1, -2 and -3, and of the cathelicidin, LL-37, were examined by real-time reverse transcription-polymerase chain reaction, and the accumulated interleukin-8 and interleukin-1 alpha were measured by enzyme-linked immunosorbent assay. Results: Nonperiodontopathic bacteria up-regulated some antimicrobial peptides without affecting the levels of cytokines. In the periodontopathic group, the orange-complex bacteria induced antimicrobial peptides and interleukin-8 efficiently, but the red-complex bacteria often demonstrated suppressive effects. In contrast to live bacteria, bacterial lysates had no suppressive effects. In addition, some bacterial lysates demonstrated a reduced ability to induce antimicrobial peptides compared with live bacteria. Conclusion: The nonperiodontopathic, the orange-complex, and the red-complex bacteria had different effects on the innate immune responses from gingival epithelial cells, which may affect the outcome of their host-microbial interaction in gingival sulcus.
ISSN
0022-3484
URI
https://hdl.handle.net/10371/190790
DOI
https://doi.org/10.1111/j.1600-0765.2007.00974.x
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