RECOMBINANT MURINE INTERLEUKIN-1-ALPHA ENHANCEMENT OF NONSPECIFIC ANTIBACTERIAL RESISTANCE
RECOMBINANT MURINE INTERLEUKIN-1-ALPHA ENHANCEMENT OF NONSPECIFIC ANTIBACTERIAL RESISTANCE
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DOI：
10.1128/iai.55.9.2061-2065.1987
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发表时间：
1987-09-01
影响因子：
3.1
通讯作者：
BROWN, JF
中科院分区：
文献类型：
--
作者：
CZUPRYNSKI, CJ;BROWN, JF
In this study we report that treatment with recombinant murine interleukin-1.alpha. (rIL-1.alpha.) significantly enhanced the resistance of mice to infection by the facultative intracellular pathogen Listeria monocytogenes. The greatest level of protection was observed at a dose of 1,000 lymphocyte-activating factor units (approximately 0.17 .mu.g) of rIL-1.alpha. per mouse. Although rIL-1.alpha. enhanced antibacterial resistance when administered either intravenously or intraperitoneally, greater protection was observed when the rIL-1.alpha. and the L. monocytogenes challenge were given by the same parenteral route. When the intravenous route was used, antibacterial resistance was maximal when the rIL-1.alpha. and L. monocytogenes were injected concomitantly. In contrast, intraperitoneal administration of rIL-1.alpha. was most effective when given 48 h before an intraperitoneal L. monocytogenes challenge. Based on the following lines of evidence, we concluded that contaminating lipopolysaccharide (LPS) was unlikely to be responsible for the enhanced antibacterial resistance that was observed: (i) LPS was not detectable ( < 0.2 ng/ml by the lysate assay) at the concentration of rIL-1.alpha. that was injected; (ii) polymyxin B did not abrogate rIL-1.alpha.-enhanced antibacterial resistance; (iii) rIL-1.alpha. treatment enhanced the antibacterial resistance of LPS-nonresponsive C3H/HeJ mice; and (iv) injection of up to 10 .mu.g of LPS per mouse (calculated to be greater than 50,000 times the concentration of LPS in the rIL-1.alpha. administered) failed to duplicate the marked enhancement of antibacterial resistance that was mediated by rIL-1.alpha.. These data provide evidence for the beneficial role of IL-1 in nonspecific antibacterial resistance.
