Monomeric IgE and lipopolysaccharide synergistically prevent mast-cell apoptosis
Monomeric IgE and lipopolysaccharide synergistically prevent mast-cell apoptosis
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DOI：
10.1016/j.bbrc.2007.10.136
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发表时间：
2008-01-04
影响因子：
3.1
通讯作者：
Ogawa, Hideoki
中科院分区：
文献类型：
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作者：
Jayawardana, Sumanasiri T. M.;Ushio, Hiroko;Ogawa, Hideoki
在无抗原存在的情况下，高浓度的IgE可显著阻止生长因子撤药后骨髓源性肥大细胞（BMMCs）的凋亡，并通过Toll样受体4（TLR 4）配体脂多糖（LPS）的存在进一步增强。LPS的作用是由TLR 4介导的，因为TLR 4缺陷的BMMCs与IgE没有显示出协同作用。中和量的抗IL-3没有逆转IgE和与LPS组合的抗凋亡作用。LPS治疗与单体IgE协同防止线粒体膜电位的损失，并与抗凋亡蛋白，Bcl-xL的表达增强，或与减少表达的促凋亡蛋白，彪马，Bim，分别。总之，这些结果表明，LPS，在TLR 4依赖的方式，与IgE一起，协同防止肥大细胞凋亡，并可能有助于调节组织肥大细胞的数量。(c)2007年爱思唯尔公司All rights reserved.
The apoptosis of bone marrow-derived mast-cells (BMMCs) after growth factor withdrawal was significantly prevented by a high concentration of IgE in the absence of antigen, and further enhanced by the presence of Toll-like receptor4 (TLR4) ligand, lipopolysaccharide (LPS). The effect of LPS was mediated by TLR4, since TLR4-deficient BMMCs did not show synergistic effects with IgE. The neutralizing amount of anti-IL-3 did not reverse the anti-apoptotic effects of both IgE and combination with LPS. LPS treatment with monomeric IgE synergistically prevented the loss of mitochondrial membrane potentials and was associated with an enhanced expression of anti-apoptotic protein, Bcl-xL, or with a reduced expression of proapoptotic protein, Puma, and Bim, respectively. Altogether, these results suggest that LPS, in a TLR4-dependent manner, together with IgE, synergistically prevent mast-cell apoptosis and may contribute to regulate the tissue mast-cell number. (c) 2007 Elsevier Inc. All rights reserved.