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


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.


CONCLUSIONS
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.
Ji
S
S
Department of Oromaxillofacial Infection & Immunity, School of Dentistry and Dental Research Institute, Seoul National University, Jongno-gu, Seoul, Korea.
Kim
Y
Y
Min
B-M
BM
Han
S H
SH
Choi
Y
Y
D001439:Bacteroides / Q000276:immunology; D002461:Cell Line, Transformed; D018920:Coculture Techniques; D015169:Colony Count, Microbial; D023082:Defensins / Q000096:biosynthesis*; D016967:Fusobacterium nucleatum / Q000276:immunology; D005881:Gingiva / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D053582:Interleukin-1alpha / Q000096:biosynthesis; D015851:Interleukin-7 / Q000096:biosynthesis; D015603:Keratinocytes / Q000276:immunology* / Q000378:metabolism; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000276:immunology; D018713:Prevotella intermedia / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D054773:Streptococcus gordonii / Q000276:immunology; D013298:Streptococcus sanguis / Q000276:immunology; D048373:Treponema denticola / Q000276:immunology; D014678:Veillonella / Q000276:immunology
D023082:Defensins; D053582:Interleukin-1alpha; D015851:Interleukin-7