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-Deficient Mice by a Concomitant Reduction of TNF-
, IL-12, and IL-18 Production1
,**,
*
First Department of Internal Medicine,
Department of Hygiene,
Second Department of Pathology, School of Medicine, and
§
Department of Molecular Pharmacology, Cancer Research Institute, Kanazawa University, Kanazawa, Japan;
¶
Department of Immunology and Medical Zoology,
||
Laboratory of Host Defenses, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo, Japan;
#
Laboratory Animal Research Center, Institute of Medical Science,
**
Molecular Preventive Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; and
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo, Japan
The present study was designed to investigate the role of IFN-
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 (M
)
and lymphocytes predominantly infiltrated the portal area, resulting in
the intrahepatic formation of granulomas consisting of epithelioid and
lymphoid cells. In comparison, in IFN- gene-disrupted BALB/c mice
(IFN- knockout mice), the number of infiltrated M 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-
, IL-12, and IL-18 and subsequently of alanine
transferase. In contrast, IFN- knockout mice developed scattered
focal necrosis of the liver with significantly lower levels of serum
alanine transferase as well as drastic decreases in TNF-, IL-12, and
IL-18 production. The administration of an anti-IFN-
neutralizing mAb at the eliciting phase significantly alleviated liver
injury and reduced serum IL-12 and IL-18 levels. Thus, endogenously
produced IFN- is involved in the pathogenesis of this liver injury
model by regulating M infiltration and granuloma formation in the
priming phase as well as cytokine production in the eliciting
phase.
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