Table 2.

Inflammatory mediator expression in serum

Inflammatory markers	Fold induction following P. gin-givalis infection1	Fold reduction following P. gingivalis infection in TLR2-deficient mice2
Interleukins
IL-1β	NS	1.6
IL-2	NS	1.5
IL-6	1.6	1.9
Chemokines
Eotaxin	NS	1.6
Lymphotactin	NS	1.5
TNF superfamily
TNF-α	NS	1.5
Fas L	NS	2.0
CD30L	1.7	1.8
sTNFRI	NS	1.7
TIMP superfamily
TIMP-1	2.3	1.7
TIMP-1	2.3	1.7

Pooled serum was examined as described in ‘Materials and Methods' using semi-quantitative membrane-based Raybio mouse inflammation antibody arrays (Raybiotech Inc.) to detect and evaluate a panel of 40 inflammatory mediators. The intensity of signals was quantified by densitometry and fold differences were determined. NS = Fold change was less than 1.5. The fold changes of eotaxin-2, fractalkine, GCSF, GM-CSF, IFN-7, IL-la, IL-3, IL-4, IL-9, IL-10, IL-12p40p70, IL-12p70, IL-13, IL-17,1-TAC, KC, Leptin, LIX, MCP-1, MCSF, MIG, MlP-la, MIP-I7, RANTES, SDF-1, TCA-3, TECK, TIMP-2 and sTNFRII were less than 1.5.

¹Fold induction in inflammatory mediators in serum ob tained from P. gingivalis-infected ApoE^−/- mice with respect to uninfected ApoE^−/- mice.

²Fold reduction in P. gingivalis-infected ApoE^−/- TLR2^−/- with respect to P. gingivalis-infected ApoE^−/- mice.