Gingival Epithelial Cells Increase Interleukin-8 Secretion in Response to Actinobacillus actinomycetemcomitans Challenge

George Huang, Susan Kinder Haake, No Hee Park

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

PERIODONTAL DISEASES RESULT FROM THE INTERACTION of bacterial pathogens with the host gingival tissues. The role of gingival epithelial cells in the initiation of host defense mechanisms after encountering oral bacteria has not been investigated. Actinobacillus actinomycetemcomitans is a key periodontal pathogen that adheres to and invades oral epithelial cells. Thus, we examined whether gingival epithelial cells increase secretion of the potent neutrophil chemoattractant interleukin-8 (IL-8) following A. actinomycetemcomitans challenge. Normal human oral keratinocytes (NHOK), isolated from gingival tissue, and 3 oral epithelial cell lines (HOK-18A, HOK-16B-BaP-T1, and HEp-2) were co-cultured with A. actinomycetemcomitans for 2 hours to allow bacteria-epithelial cell interactions. The epithelial cells were then washed, and fresh medium with gentamicin was added to kill extracellular bacteria. Cell cultures were further incubated for 24 hours before the supernatant was collected for IL-8 detection with ELISA. The results showed that IL-8 secretion increased 2- to 7-fold 24 hours after bacterial challenge. The highest IL-8 secretion was at the multiplicity of infection (MOI) of 1,000:1 in bacterial dose response studies using HOK-16B-BaP-T1 cells. Time-course studies revealed that IL-8 secretion rapidly reached a maximum level 6 hours after bacterial challenge and subsequently decreased to basal levels. These data indicate that gingival epithelial cells are capable of upregulating IL-8 expression rapidly in response to A. actinomycetemcomitans challenge and thus may facilitate the recruitment of neutrophils as a host defense mechanism.

Original languageEnglish (US)
Pages (from-to)1105-1110
Number of pages6
JournalJournal of Periodontology
Volume69
Issue number10
DOIs
StatePublished - Jan 1 1998
Externally publishedYes

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Aggregatibacter actinomycetemcomitans
Interleukin-8
Epithelial Cells
Bacteria
Neutrophil Infiltration
Chemotactic Factors
Periodontal Diseases
Gentamicins
Keratinocytes
Cell Communication
Neutrophils
Cell Culture Techniques
Enzyme-Linked Immunosorbent Assay
Cell Line
Infection

All Science Journal Classification (ASJC) codes

  • Periodontics

Cite this

Gingival Epithelial Cells Increase Interleukin-8 Secretion in Response to Actinobacillus actinomycetemcomitans Challenge. / Huang, George; Haake, Susan Kinder; Park, No Hee.

In: Journal of Periodontology, Vol. 69, No. 10, 01.01.1998, p. 1105-1110.

Research output: Contribution to journalArticle

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abstract = "PERIODONTAL DISEASES RESULT FROM THE INTERACTION of bacterial pathogens with the host gingival tissues. The role of gingival epithelial cells in the initiation of host defense mechanisms after encountering oral bacteria has not been investigated. Actinobacillus actinomycetemcomitans is a key periodontal pathogen that adheres to and invades oral epithelial cells. Thus, we examined whether gingival epithelial cells increase secretion of the potent neutrophil chemoattractant interleukin-8 (IL-8) following A. actinomycetemcomitans challenge. Normal human oral keratinocytes (NHOK), isolated from gingival tissue, and 3 oral epithelial cell lines (HOK-18A, HOK-16B-BaP-T1, and HEp-2) were co-cultured with A. actinomycetemcomitans for 2 hours to allow bacteria-epithelial cell interactions. The epithelial cells were then washed, and fresh medium with gentamicin was added to kill extracellular bacteria. Cell cultures were further incubated for 24 hours before the supernatant was collected for IL-8 detection with ELISA. The results showed that IL-8 secretion increased 2- to 7-fold 24 hours after bacterial challenge. The highest IL-8 secretion was at the multiplicity of infection (MOI) of 1,000:1 in bacterial dose response studies using HOK-16B-BaP-T1 cells. Time-course studies revealed that IL-8 secretion rapidly reached a maximum level 6 hours after bacterial challenge and subsequently decreased to basal levels. These data indicate that gingival epithelial cells are capable of upregulating IL-8 expression rapidly in response to A. actinomycetemcomitans challenge and thus may facilitate the recruitment of neutrophils as a host defense mechanism.",
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