Membrane changes in lipopolysaccharide-stimulated murine B lymphocytes associated with cell activation.
Membrane changes in lipopolysaccharide-stimulated murine B lymphocytes associated with cell activation.
复制标题
脂多糖刺激的鼠 B 淋巴细胞的膜变化与细胞活化相关。
DOI：
10.1016/0005-2736(93)90164-u
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Barisas,BG
中科院分区：
文献类型：
--
作者：
Printen,JA;Woodard,SL;Herman,JR;Roess,DA;Barisas,BG
The lateral diffusion of the fluorescent lipid analog 3,3′-dioctadecylindocarbocyanine iodide (DiI) was measured in the membranes of murine B lymphocytes treated with the B cell mitogen lipopolysaccharide (LPS). The mobility of DiI, as measured by fluorescence photobleaching recovery (FPR) techniques, was temperature-dependent with a value of 6.1 · 10−9cm2s−1at 37°C. Untreated cells exhibited this diffusion coefficient over 72 h in culture. In contrast, DiI mobility decreased to 2.0 · 10−9cm2s−1at 37°C in membranes of LPS-stimulated lymphocytes 24 h following LPS exposure. Interestingly, this decreased lipid lateral diffusion was not accompanied by any change in surface immunoglobulin lateral diffusion which remained essentially unchanged at 3.6-4.3 · 10−11cm2s−1over 72 h. To determine whether LPS effects on lipid lateral diffusion were due to insertion of LPS into the cell plasma membrane, we examined TRITC-LPS diffusion in B lymphocytes from LPS-responsive Balb/c and C3Heb/FeJ mice and from hypo-responsive C3H/HeJ mice. DiI and TRITC-LPS mobility decreased more than 50% in LPS-stimulated Balb/c and C3Heb/FeJ cells by 72 h. On C3H/HeJ lymphocytes, there was no change in DiI or TRITC-LPS lateral diffusion throughout the incubation period. These data indicate that B lymphocyte membrane compositions is altered in LPS-activated lymphoblasts and that the decreased lateral diffusion of lipid probes does not result from membrane perturbation by LPS insertion into the lipid bilayer. Further, similarities between TRITC-LPS and DiI lateral diffusion suggest that most LPS molecules interact non-specifically with B cell membranes, presumably by acyl chain insertion of the lipid A moiety.
