Strain-Dependent Cytokine Profile and Susceptibility to Oleic Acid Anilide in a Murine Model of the Toxic Oil Syndrome

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• 作者：Berking ; Carola ; Hobbs ; Monte V. ; Chatelain ; René ; Meurer ; Michael ; Bell ; Susanne A.
• 刊名：Toxicology and Applied Pharmacology
• 出版年：1998
• 出版时间：February, 1998
• 年：1998
• 卷：148
• 期：2
• 页码：222-228
• 全文大小：229 K

文摘

The toxic oil syndrome (TOS) was caused by the ingestion of an adulterated rapeseed oil containing oleic acid anilide (OAA). It was characterized by lethal symptoms in the acute phase and by symptoms of idiopathic autoimmune diseases in the chronic phase. The pathogenetic mechanisms remain unclear. In a murine model of TOS we demonstrate strain-dependent effects on the immune system after treatment with OAA intraperitoneally. While C57BL/6 (H-2b) mice develop a polyclonal B cell activation without disease symptoms, most A/J (H-2a) mice suffer an acute lethal wasting disease. These differences are reflected in the splenic cytokine gene expression and secretion and in the Ig production. Increased IgE serum levels and reduced TNF-β mRNA suggest a Th2 cell response in C57BL/6 mice. In A/J mice, splenocytes express IL-1α, IL-10, and IFN-γ mRNAin vivoand secrete high levels of TNF-αin vitro. These observations resemble the human condition in TOS with development of either an acute lethal disease or a chronic autoimmune-like disease. As in other chemical-induced reactions genetic susceptibility seems to be important.