Figure 5
LCMV-induced liver damage shows distinct phases of fibrosis and resolution improved by ruxolitinib therapy. (A) Histological analysis of hepatic fibrosis using PicroSirius red staining (upper) and Masson’s Trichome (lower) from nontreated control mice (B6) (days 11 and 28) and Prf1−/− mice either nontreated (day 11) or treated with ruxolitinib and analyzed at day 28 postinfection. One representative of at least 5 randomly chosen fields is shown. (B, left) Liver size and (right) absolute number of MNCs in the liver of control (B6) and Prf1−/− mice nontreated or treated for 14 days from day 7 postinfection. (C) Relative expression of Ifnγ, Nos2, Chil3, and Il10 in liver MNCs obtained before or after LCMV infection in control (B6) and Prf1−/− mice either nontreated or treated with ruxolitinib. Data (mean ± SEM) are representative of 2 independent experiments with at least 3 mice in each group. *P < .05; **P < .005; ***P < .001.

LCMV-induced liver damage shows distinct phases of fibrosis and resolution improved by ruxolitinib therapy. (A) Histological analysis of hepatic fibrosis using PicroSirius red staining (upper) and Masson’s Trichome (lower) from nontreated control mice (B6) (days 11 and 28) and Prf1−/− mice either nontreated (day 11) or treated with ruxolitinib and analyzed at day 28 postinfection. One representative of at least 5 randomly chosen fields is shown. (B, left) Liver size and (right) absolute number of MNCs in the liver of control (B6) and Prf1−/− mice nontreated or treated for 14 days from day 7 postinfection. (C) Relative expression of Ifnγ, Nos2, Chil3, and Il10 in liver MNCs obtained before or after LCMV infection in control (B6) and Prf1−/− mice either nontreated or treated with ruxolitinib. Data (mean ± SEM) are representative of 2 independent experiments with at least 3 mice in each group. *P < .05; **P < .005; ***P < .001.

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