Malagoli Davide, Ottaviani Enzo
Department of Animal Biology, University of Modena and Reggio Emilia, via Campi 213/D, 41100 Modena, Italy.
Cell Biol Int. 2004;28(1):57-61. doi: 10.1016/j.cellbi.2003.10.003.
Using computer-assisted microscopic image analysis, we have found that algal yessotoxin (YTX) affects the immune response of Mytilus galloprovincialis. Indeed, YTX increases immunocyte cell motility through the involvement of both extracellular Ca2+ and cAMP, but not through protein kinase A, protein kinase C or phosphoinositide 3-kinase. Alone, however, the toxin does not induce any effect, as its action on cell motility is observed only after addition of the chemotactic substance N-formyl-Meth-Leu-Phe (fMLP). fMLP is known to induce cellular changes via both the phosphatidylinositol and cAMP pathways and, from this scenario, we can surmise that Ca2+ and cAMP concentrations rise sufficiently in fMLP-activated immunocytes to reveal YTX action. One possible explanation is that the toxin increases fMLP-mediated cell activation by intervening in L-type Ca2+-channel opening through a cAMP-dependent/PKA-independent pathway.
通过计算机辅助显微镜图像分析，我们发现藻类产生的虾夷毒素（YTX）会影响地中海贻贝的免疫反应。实际上，YTX通过细胞外Ca2+和cAMP的参与来增加免疫细胞的运动性，但不是通过蛋白激酶A、蛋白激酶C或磷脂酰肌醇3激酶。然而，单独的毒素不会产生任何影响，因为只有在添加趋化物质N-甲酰甲硫氨酰亮氨酰苯丙氨酸（fMLP）后，才能观察到其对细胞运动性的作用。已知fMLP通过磷脂酰肌醇和cAMP途径诱导细胞变化，从这种情况来看，我们可以推测在fMLP激活的免疫细胞中Ca2+和cAMP浓度会充分升高，从而揭示YTX的作用。一种可能的解释是，该毒素通过cAMP依赖/蛋白激酶A非依赖途径干预L型Ca2+通道开放，从而增强fMLP介导的细胞激活。
