Abstract

We examined the effect of Bisphenol A (BPA) on non-specific defense in experiments with a non-pathogenic bacterium, Escherichia coli K-12. Mice were pretreated by a subcutaneous route with BPA (5 mg/kg body weight) for 5 consecutive days in the back and 3 days after the last treatment, injected by the intra-peritoneal route with E. coli K-12. BPA pretreatment caused a decrease of T and B cell populations in the spleen of treated mice. After the challenge with E. coli, the activity to eliminate bacteria from the peritoneal cavity in the early stage of infection (within 24 h) was diminished compared with non-treated mice. BPA induced the migration of excess neutrophils into the peritoneal cavity, but reduced their phagocytic activity against E. coli K-12. For macrophages and lymphocytes, BPA reduced the population in the spleen and the accumulation at infection foci. The production of MCP-1 was enhanced by BPA treatment, but that of IL-6 was suppressed after infection. These results suggest that BPA possessed immunotoxicity and reduced the non-specific host defense as an acute toxicity.

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