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Journal of Dental Research
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VIP Inhibits P. gingivalis LPS-induced IL-18 and IL-18BPa in Monocytes

N. Foster1, K. Andreadou, L. Jamieson, P.M. Preshaw and J.J. Taylor2

Oral Microbiology and Host Responses Group, Oral Biology, School of Dental Sciences, University of Newcastle upon Tyne, NE2 4BW, UK


Figure 1
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  		Figure 1. Pg LPS stimulated IL-18 and IL-18BPa production by THP1 monocytes. (A) Pg and E. coli LPS (100 ng/mL) increased IL-18 production in THP1 monocytes after 6–24 hrs. (B) Pg and E. coli LPS (100 ng/mL) increased IL-18BPa production in THP1 monocytes after 6–24 hrs. IL-18 and IL-18BPa levels were measured by ELISA and compared with unstimulated cells (controls). Each value is a mean (± SD) of 3 experiments recorded on 3 separate occasions. *p < 0.05 compared with controls.

 

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  		Figure 2. Interaction of IL-18BPa with IL-18 in THP1 culture supernatants. Co-culture of anti-IL-18BPa antibodies with THP1 monocytes in the presence of Pg LPS (100 ng/mL) for 24 hrs significantly increased the concentration of free IL-18 measured in cell supernatants, compared with antibody-free controls. IL-18BPa levels were measured by ELISA. Each value is a mean (± SD) of 3 experiments recorded on 3 separate occasions. *p < 0.05 compared with controls.

 

Figure 3
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  		Figure 3. VIP inhibited Pg LPS-stimulated IL-18 and IL-18BPa production by THP1 monocytes. (A) VIP (10–8 M) inhibited Pg LPS (100 ng/mL)-stimulated IL-18 production in THP1 monocytes cultured for 6-48 hrs. (B) VIP (10–8 M) inhibited Pg LPS (100 ng/mL)-stimulated IL-18BPa production in THP1 monocytes cultured for 6-48 hrs. IL-18 and IL-18BPa levels were measured by ELISA. Each value is a mean (± SD) of 3 experiments recorded on 3 separate occasions. *p < 0.05 compared with cells stimulated with LPS in the absence of VIP.

 

Journal of Dental Research, Vol. 86, No. 9, 883-887 (2007)
DOI: 10.1177/154405910708600915
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