Vogel S N, Weedon L L, Oppenheim J J, Rosenstreich D L
J Immunol. 1981 Feb;126(2):441-5.
Peritoneal macrophages from LPS hyporesponsive C3H/HeJ mice lose the capacity to bind and phagocytose opsonized sheep erythrocytes (EA) over a 48-hr culture period. This loss in Fc receptor capacity is markedly different from the progressive increase in phagocytic ability exhibited by cultured macrophages derived from LPS-responsive C3H/HeN mice. Since dibutyryl-cyclic adenosine monophosphate (DBcAMP) has previously been reported to modulate membrane receptor expression in lymphocytes and certain macrophage-like cell lines, we examined its effects on EA binding and phagocytosis by C3H/HeJ macrophages. DBcAMP not only reverses the binding defect in C3H/HeJ macrophages but also restores EA phagocytosis to the level of control C3H/HeN cultures. 8-Bromo-cAMP, as well as other agents known to elevate intracellular cAMP (i.e., isoproterenol plus isobutylmethylxanthine or prostaglandin E2) also corrected the phagocytic defect. Since the C3H/HeJ macrophage phagocytic defect can also be reversed by in vitro stimulation with a lymphokine-rich culture supernatant, we examined the effect of this treatment on intracellular cAMP levels. Lymphokine treatment produced a 60% increase in the levels of macrophage intracellular cAMP. These findings suggest that the C3H/HeJ differentiation defect may be secondary to some abnormality in a cAMP dependent pathway.
来自脂多糖低反应性C3H/HeJ小鼠的腹腔巨噬细胞在48小时的培养期内丧失了结合和吞噬调理过的绵羊红细胞（EA）的能力。Fc受体能力的这种丧失与来自脂多糖反应性C3H/HeN小鼠的培养巨噬细胞所表现出的吞噬能力的逐渐增加明显不同。由于先前已报道二丁酰环磷酸腺苷（DBcAMP）可调节淋巴细胞和某些巨噬细胞样细胞系中的膜受体表达，我们研究了其对C3H/HeJ巨噬细胞EA结合和吞噬作用的影响。DBcAMP不仅逆转了C3H/HeJ巨噬细胞的结合缺陷，还将EA吞噬作用恢复到对照C3H/HeN培养物的水平。8-溴环磷酸腺苷以及其他已知可提高细胞内cAMP的试剂（即异丙肾上腺素加异丁基甲基黄嘌呤或前列腺素E2）也纠正了吞噬缺陷。由于富含淋巴因子的培养上清液的体外刺激也可逆转C3H/HeJ巨噬细胞的吞噬缺陷，我们研究了这种处理对细胞内cAMP水平的影响。淋巴因子处理使巨噬细胞内cAMP水平增加了60%。这些发现表明，C3H/HeJ分化缺陷可能继发于cAMP依赖性途径中的某些异常。
