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. 2014 Dec 22;125(2):539–550. doi: 10.1172/JCI76887

Figure 4. HMGB1 does not modulate inflammation, injury, or survival in response to FAS- or TNF-induced apoptosis.

Figure 4

(A and B) Hepatic inflammatory gene expression (A) and neutrophil infiltration (B) 10 hours after injection of a sublethal dose of the FAS-agonistic antibody Jo2 (0.15 μg/g) in Hmgb1fl/fl (n = 6) and Hmgb1Δhep (n = 7) mice. (C) Hepatic H&E staining and hemorrhage 5 hours after a lethal dose of Jo2 (0.5 μg/g) in Hmgb1fl/fl and Hmgb1Δhep (n = 3 per group) mice. (D and E) Serum ALT after 5 hours (D) and survival (E) in Hmgb1fl/fl (n = 9) and Hmgb1Δhep (n = 10) mice after Jo2 injection (0.5 μg/g). (FJ) Mice were injected with 700 μg/kg D-Gal and 100 μg/kg LPS. Hepatic inflammatory gene expression (F), neutrophil infiltration (G), hemorrhage (H), and serum ALT (I) 6 hours later in Hmgb1fl/fl and Hmgb1Δhep (n = 5 per group) mice. (J) Survival of Hmgb1fl/fl and Hmgb1Δhep (n = 10 per group) mice. Statistical significance assessed by 2-tailed unpaired t test (AD and FI) and Mantel-Cox log-rank test (E and J). Scale bars: 200 μm (B, C, G, and H).