Iida M, Hirai K, Shinohara S, Yamaguchi M, Takaishi T, Sakamoto Y, Ito K, Morita Y
Department of Medicine and Physical Therapy, University of Tokyo School of Medicine, Japan.
Biochem Biophys Res Commun. 1994 Sep 15;203(2):1295-301. doi: 10.1006/bbrc.1994.2323.
Lipopolysaccharide (LPS) is known to enhance IgE-mediated basophil degranulation. Recently, the complex of LPS and plasma LPS-binding protein(LBP) has been shown to induce secretory response via CD14 in monocytes and neutrophils. In the current study, we observed that the sensitivity to LPS of basophils was increased to 100-fold by co-incubation with plasma. LPS promptly completed its effect and amplified degranulation by stimuli bypassing IgE-receptors. Treatment with anti-CD14 completely abolished the priming effect of LPS. These results indicate that the priming effect of LPS on basophil mediator release is mediated via CD14, and that plasma co-factor, possibly identical to LBP, potentiates this reaction.
已知脂多糖(LPS)可增强IgE介导的嗜碱性粒细胞脱颗粒。最近,LPS与血浆LPS结合蛋白(LBP)的复合物已被证明可通过单核细胞和中性粒细胞中的CD14诱导分泌反应。在本研究中,我们观察到,与血浆共同孵育后,嗜碱性粒细胞对LPS的敏感性提高了100倍。LPS迅速发挥其作用,并通过绕过IgE受体的刺激放大脱颗粒。用抗CD14治疗可完全消除LPS的启动作用。这些结果表明,LPS对嗜碱性粒细胞介质释放的启动作用是通过CD14介导的,并且血浆辅助因子(可能与LBP相同)可增强这种反应。