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• W4313331693 abstract "Abstract The present study was designed to investigate the role of IFN-γ in LPS-induced liver injury following priming with Propionibacterium acnes. At 1 week after priming BALB/c mice with P. acnes, a large number of macrophages (Mφ) and lymphocytes predominantly infiltrated the portal area, resulting in the intrahepatic formation of granulomas consisting of epithelioid and lymphoid cells. In comparison, in IFN-γ gene-disrupted BALB/c mice (IFN-γ knockout mice), the number of infiltrated Mφ was decreased, with a significant reduction in the number and size of granulomas. Subsequent elicitation with a low dose of LPS induced massive hepatic necrosis in wild-type BALB/c mice, with a marked increase in the serum levels of TNF-α, IL-12, and IL-18 and subsequently of alanine transferase. In contrast, IFN-γ knockout mice developed scattered focal necrosis of the liver with significantly lower levels of serum alanine transferase as well as drastic decreases in TNF-α, IL-12, and IL-18 production. The administration of an anti-IFN-γ neutralizing mAb at the eliciting phase significantly alleviated liver injury and reduced serum IL-12 and IL-18 levels. Thus, endogenously produced IFN-γ is involved in the pathogenesis of this liver injury model by regulating Mφ infiltration and granuloma formation in the priming phase as well as cytokine production in the eliciting phase." @default.
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• W4313331693 date "1999-01-15" @default.
• W4313331693 modified "2023-10-10" @default.
• W4313331693 title "Alleviation of Lipopolysaccharide-Induced Acute Liver Injury in<i>Propionibacterium acnes</i>-Primed IFN-γ-Deficient Mice by a Concomitant Reduction of TNF-α, IL-12, and IL-18 Production" @default.
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• W4313331693 doi "https://doi.org/10.4049/jimmunol.162.2.1049" @default.
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