CD14参与脂多糖诱导人单核细胞和肺泡巨噬细胞释放肿瘤坏死因子-α、白细胞介素-6和白细胞介素-8 。
Involvement of CD14 in lipopolysaccharide-induced tumor necrosis factor-alpha, IL-6 and IL-8 release by human monocytes and alveolar macrophages.
作者信息
Dentener M A, Bazil V, Von Asmuth E J, Ceska M, Buurman W A
机构信息
Department of Surgery, University of Limburg, Maastricht, The Netherlands.
出版信息
J Immunol. 1993 Apr 1;150(7):2885-91.
CD14 has been reported to function as a receptor for bacterial LPS complexed with serum proteins, transducing an activation signal for TNF-alpha production. We found that the anti-CD14 mAb MEM-18 inhibited not only LPS-induced release of TNF-alpha, but also LPS-induced, TNF-alpha independent release of IL-6 and IL-8 by human monocytes and alveolar macrophages. Inhibitory effect of MEM-18 was detected both in the presence of human or bovine calf serum and under serum-free conditions. In contrast, MEM-18 did not block release of these cytokines induced by IL-1 beta, TNF-alpha, PMA, and zymosan. We conclude that CD14 is involved in LPS-induced release of TNF-alpha, IL-6, and IL-8 by monocytes and alveolar macrophages and that this receptor appears to be able to recognize LPS directly in the absence of serum.
据报道，CD14作为与血清蛋白复合的细菌脂多糖（LPS）的受体发挥作用，转导肿瘤坏死因子-α（TNF-α）产生的激活信号。我们发现，抗CD14单克隆抗体MEM-18不仅抑制LPS诱导的TNF-α释放，还抑制LPS诱导的人单核细胞和肺泡巨噬细胞释放白细胞介素-6（IL-6）和白细胞介素-8（IL-8），且这种释放不依赖于TNF-α。在存在人或小牛血清的情况下以及无血清条件下，均检测到MEM-18的抑制作用。相比之下，MEM-18并不阻断由白细胞介素-1β（IL-1β）、TNF-α、佛波酯（PMA）和酵母聚糖诱导的这些细胞因子的释放。我们得出结论，CD14参与单核细胞和肺泡巨噬细胞LPS诱导的TNF-α、IL-6和IL-8释放，并且该受体似乎能够在无血清的情况下直接识别LPS。
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