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. 2012 Jun 22;7(6):e39155. doi: 10.1371/journal.pone.0039155

Figure 2. Delayed development of P. acnes effects in primed TLR9−/− mice.

Figure 2

Groups of WT and TLR9−/− mice (15–20 animals/group) were primed with heat-killed P. acnes (20 µg/g b.w.) i.v. or remained untreated (controls; day 0). A. Hypersensitivity to LPS: At indicated time points after priming the animals were challenged with LPS from S.a.e. (0.01 µg/g b.w.), i.v. One hour and 4 h later, plasma was collected for determination of TNF-α and IFN-γ, respectively. Before challenge with LPS no detectable TNF-α or IFN-γ was found in plasma of P. acnes-treated mice of either one of the groups (not shown). Cumulative data of 3 different experiments are shown. *:p-value<0.05 and ***:p-value<0.001 WT compared to TLR9−/− mice, and P. acnes-treated WT or P. acnes-treated TLR9−/− at the indicated time point compared to untreated controls. B. Splenomegaly: Spleens were removed and weighted at indicated time points after treatment. Cumulative data from 4–5 experiments are shown. *:p-value<0.05 and **:p-value<0.01. C. Enhanced resistance to serovar Typhimurium infection is delayed in TLR9−/− mice: 7 or 21 days after priming, the animals were infected with Salmonella serovar Typhimurium (200 CFU/0.2 ml PBS/i.v.). Bacterial counts in liver of unprimed and primed animals were determined 4 days after infection. One representative experiment of three is shown. *:p-value<0.05 and **:p-value<0.01.