Dramsi Shaynoor, Cossart Pascale
Unité des Interactions Bactéries-Cellules, Institut Pasteur, 75724 Paris Cedex 15, France.
Infect Immun. 2003 Jun;71(6):3614-8. doi: 10.1128/IAI.71.6.3614-3618.2003.
To investigate factors which modulate the entry of Listeria monocytogenes into mammalian cells, we have analyzed the role of Ca(2+). We show that L. monocytogenes induced Ca(2+) transients into the human Hep-2 epithelial cell line. The nonpathogenic species L. innocua or a L. monocytogenes mutant strain defective in listeriolysin O (LLO) production was unable to induce these calcium fluxes. Addition of plasma membrane calcium channel antagonists or chelation of extracellular calcium markedly reduced L. monocytogenes entry. In contrast, chelation of host cytosolic Ca(2+) or blockade of Ca(2+) release from intracellular stores did not affect invasion. These results indicate that L. monocytogenes-induced mobilization of extracellular Ca(2+) by LLO and activation of downstream Ca(2+)-dependent signaling are required for efficient cell invasion.
为了研究调节单核细胞增生李斯特菌进入哺乳动物细胞的因素,我们分析了Ca(2+)的作用。我们发现,单核细胞增生李斯特菌可诱导人Hep-2上皮细胞系出现Ca(2+)瞬变。无毒李斯特菌或产单核细胞李斯特菌溶血素O(LLO)缺陷的突变菌株无法诱导这些钙通量。添加质膜钙通道拮抗剂或螯合细胞外钙可显著减少单核细胞增生李斯特菌的进入。相反,螯合宿主胞质Ca(2+)或阻断细胞内钙库释放Ca(2+)并不影响侵袭。这些结果表明,LLO诱导的细胞外Ca(2+)动员以及下游Ca(2+)依赖性信号的激活是细胞有效侵袭所必需的。