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. 2004 Apr;72(4):2131–2139. doi: 10.1128/IAI.72.4.2131-2139.2004

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FIG. 6. — Increased hepatic microabscesses in TLR2-deficient infected mice. Two days after i.v. infection with 2 × 10⁵ CFU of Listeria, the livers of infected TLR2^+/+ (A), TLR2^−/− (B), and MyD88^−/− (C) mice contained multiple microabscesses. (D) Numbers of microabscesses per 20 fields quantified and expressed as means ± SD (*, P < 0.05). Histologic samples were stained with hematoxylin and eosin (magnification, ×200). (E, F, and G) Liver microabscesses from wild-type, TLR2^−/−, and MyD88^−/− mice, respectively, at a higher magnification (×400). Results are from one representative experiment of two independent experiments.

FIG. 6. — Increased hepatic microabscesses in TLR2-deficient infected mice. Two days after i.v. infection with 2 × 10⁵ CFU of Listeria, the livers of infected TLR2^+/+ (A), TLR2^−/− (B), and MyD88^−/− (C) mice contained multiple microabscesses. (D) Numbers of microabscesses per 20 fields quantified and expressed as means ± SD (*, P < 0.05). Histologic samples were stained with hematoxylin and eosin (magnification, ×200). (E, F, and G) Liver microabscesses from wild-type, TLR2^−/−, and MyD88^−/− mice, respectively, at a higher magnification (×400). Results are from one representative experiment of two independent experiments.