Iowa Section of AADR - The University of Iowa College of Dentistry

phenotypes are currently being evaluated and will be presented.
Supported by: CDC grant 5R01DD000295; R03-AR055313; NIDCR Training Grant T32 DE014678-09
3. HBD3-enhanced Porphyromonas gingivalis rHagB Cytokine Responses in Dendritic Cells
L. Harvey 1 , K.A. Brogden 1 , A. Progulske-Fox 6
1 University of Iowa; 6 University of Florida, Gainesville, FL
Previously, we found that HBD3, co-administered with recombinant hemagglutinin B (rHagB) attenuates a
Porphyromonas gingivalis rHagB in human myeloid dendritic
cells.
Objectives: The objective of this study was to determine if the chemokine and cytokine response of dendritic cells
induced by rHagB is still attenuated when HBD3 is administered prior to exposure with rHagB; when administered
simultaneously with rHagB; or when administered after exposure to rHagB.
Methods:
post exposure, culture supernatants were removed for the determination of 22 chemokines and cytokines using
Instrument (Luminex, Austin, TX).
Results: rHagB alone induced a robust chemokine and cytokine response. The timing of HBD3 administration
was important. HBD3 co-incubated with rHagB (for 30 min prior to exposure) attenuated a chemokine and
simultaneously, but not together or if HBD3 was administered 1 hour after, then rHagB induces a modestly robust
Conclusions: The results show that the timing of HBD3 administration is important and HBD3 has the capacity to
modulate the cytokine and chemokine response of dendritic cells to rHagB. Supported by funds from NIH, NIDCR
R01 DEO14390.
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Supported by: University of Iowa, College of Dentistry, Iowa Dental Research Grant
4. HBD3 Inhibits Porphyromonas gingivalis rHagB Binding to Dendritic Cells
J. Van Hemert 5 , E. Recker 5 , K. Walters 2 , A. Progulske-Fox 6 , K.A. Brogden 5
2 5 6 University of Iowa, Iowa City, IA; University of Iowa College of Dentistry, Iowa City, IA; University of Florida,
Gainesville, FL
Human β-defensin 3 (HBD3) is a small, well-characterized peptide with broad antimicrobial activities and
diverse innate immune functions. Previously, we found that HBD3 binds to recombinant Porphyromonas gingivalis
dendritic cells.
Objectives: Our objective was to determine if HBD3 binding to rHagB alters the binding of rHagB to the surface of
human myeloid dendritic cells.
Methods: To test this, human myeloid dendritic cells and mouse JAWS II cells were incubated with 0.1 μM
rHagB, 1.0 μM HBD3+0.1 μM rHagB (10:1 molar ratio), 1.0 μM HBD3, or 0.1 M PBS, pH 7.2. After 5 minutes,
with monoclonal MoAb 1858 to rHagB, polyclonal rabbit to rHagB, and polyclonal 500-P241 rabbit antibody to
microscopy.
Results: For confocal microscopy, 6.3 x 104 dendritic cells in chamber slides were incubated with rHagB and had
Conclusion: Overall, these results strongly suggest that HBD3 binding to rHagB alters the binding of rHagB to the
response of rHagB in dendritic cells. This work was supported by NIH, NIDCR grant R01 DEO14390.
Supported by: NIH, NIDCR grant R01 DEO14390.
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