Cohen L, David B, Cavaillon J M
Unité d'Immuno-Allergie, Institut Pasteur, Paris, France.
Immunol Lett. 1991 May;28(2):121-6. doi: 10.1016/0165-2478(91)90109-n.
In addition to its hematopoietic activities, interleukin-3 (IL-3) can modulate macrophage functions. We have studied the production of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (TNF) by mouse peritoneal macrophages triggered by lipopolysaccharide (LPS) in the presence or absence of IL-3. Interleukin-3 at the concentration used (i.e., 100 U/ml) did not induce the production of any cytokines, whereas it enhanced significantly the secretion of IL-1, IL-6 and TNF by LPS-stimulated macrophages. The synergistic activity of IL-3 was observed over a wide range of Escherichia coli or Salmonella enteritidis LPS concentrations. No additive effect was noticed between IL-3 and granulocyte/macrophage colony-stimulating factor (GM-CSF), another factor able to enhance LPS-induced IL-1 production. Thus, IL-3 can potentiate the inflammatory response induced by endotoxin from Gram-negative bacteria through a potentiation of cytokine production.
除了其造血活性外，白细胞介素-3（IL-3）还可调节巨噬细胞功能。我们研究了在有或无IL-3存在的情况下，脂多糖（LPS）触发的小鼠腹腔巨噬细胞产生白细胞介素-1（IL-1）、白细胞介素-6（IL-6）和肿瘤坏死因子（TNF）的情况。所用浓度（即100 U/ml）的IL-3不会诱导任何细胞因子的产生，而它能显著增强LPS刺激的巨噬细胞分泌IL-1、IL-6和TNF。在广泛的大肠杆菌或肠炎沙门氏菌LPS浓度范围内都观察到了IL-3的协同活性。在IL-3和粒细胞/巨噬细胞集落刺激因子（GM-CSF）之间未发现相加效应，GM-CSF是另一种能够增强LPS诱导的IL-1产生的因子。因此，IL-3可通过增强细胞因子产生来增强革兰氏阴性菌内毒素诱导的炎症反应。
