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Results of in vivo and in vitro experiments suggest that the early suppression of brucella growth in double stranded polyadenylic-polyuridylic acid(poly A: U-) treated mice was due to a non-specific activation of macrophages by poly A: U. Poly A: U administered intraperitoneally at the time of brucella infection failed to enhance T-cell mediated responses to the organism, namely delayed-type hypersensitivity to brucellin and adoptive transfer of immunity to the infection. Poly A: U did not augment the protective antibodies formed in response to infection. Although poly A:U has been previously found to suppress brucellosis in athymic (nude) mice, it did not enhance the thymus-dependent antibody response to sheep erythrocytes in brucella-infected nudes, suggesting that it did not significantly enhance maturation of their helper T-cell percursors. Increased macrophage spreading, an indication of activation, was seen immediately after administration of poly A: U and Brucella abortus. Later on the infection spreading was suppressed, a phenomenon which appears to relate to the biphasic effect of poly A: U in vivo described in the accompanying paper. Peritoneal macrophages treated in vitro with poly A: U were stimulated to spread on plastic surfaces, even when T lymphocytes were removed with anti-Thy-1 serum and complement. [ABSTRACT FROM AUTHOR]

The double stranded polynucleotide, poly A:U, when administered intraperitoneally at the same time as intravenous infection with Brucella abortus, suppressed the growth of that organism in the spleen and liver of mice. Single stranded poly A or poly U were not effective. On the other hand both the single and double stranded forms enhanced the growth of Br. abortus in broth culture. Poly A: U did not enhance the blood clearance of intravenously administered Br. abortus. Indeed its suppressive effect was not apparent until 2 days after administration. When mice given Br. abortus and poly A:U were given a second infection 2 days later, with either Br. abortus or Listeria monocytogenes, the second infection was exacerbated, indicating a biphasic effect of poly A: U and antigen. [ABSTRACT FROM AUTHOR]