Mattingly J A, Eardley D D, Kemp J D, Gershon R K
J Immunol. 1979 Mar;122(3):787-90.
The role of the products of prostaglandin synthetase in the suppression of in vitro secondary antibody responses by rat spleen cells was examined. By including cells from both germfree and conventional rats in these studies, the effect of in vivo microbial stimulation on this suppression was also determined. We found that 1) the suppression that is normally present in the spleen cells of rats can be eliminated by the use of glass wool or indomethacin; 2) germfree rats do not display this suppressor activity, and 3) this "deficit" in the germfree rat may be due to a lack of a microbial-induced signal from a nonadherent cell to an adherent prostaglandin-containing macrophage, implying that at least two cells are involved in the prostaglandin-synthetase dependent suppressor effect. It is possible that large amounts of some or all microbial products activate "suppressor" macrophages and that inbred rats behave like "chronically infected" mice because of an inability to regulate their "normal" microbial flora.
研究了前列腺素合成酶产物在抑制大鼠脾细胞体外二次抗体反应中的作用。通过在这些研究中纳入无菌大鼠和普通大鼠的细胞,还确定了体内微生物刺激对这种抑制作用的影响。我们发现:1)使用玻璃棉或消炎痛可消除正常存在于大鼠脾细胞中的抑制作用;2)无菌大鼠不表现出这种抑制活性;3)无菌大鼠中的这种“缺陷”可能是由于缺乏从非黏附细胞到含前列腺素的黏附巨噬细胞的微生物诱导信号,这意味着至少有两种细胞参与了依赖前列腺素合成酶的抑制作用。有可能大量的某些或所有微生物产物激活了“抑制性”巨噬细胞,并且近交系大鼠表现得像“慢性感染”的小鼠,因为它们无法调节其“正常”微生物群落。