Fujikura Daisuke, Toyomane Kochi, Kamiya Kozue, Mutoh Memi, Mifune Etsuko, Ohnuma Miyuki, Higashi Hideaki
Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University, Kita-20, Nishi-10, Kita-ku, Sapporo, Hokkaido 001-0020, Japan.
J Vet Med Sci. 2016 Sep 1;78(8):1311-7. doi: 10.1292/jvms.15-0727. Epub 2016 May 12.
Several animal models have shown that anthrax toxin (ATX) elicits a cytotoxic effect on host cells through anthrax toxin receptor (ANTXR) function. In this study, compared with mouse cells, cells obtained from humans exhibited low sensitivity to ATX-mediated cytotoxicity, and the sensitivity was not correlated with expression levels of ANTXRs. ATX treatment also induced a cytotoxic effect in other cultured human cells, human embryonic kidney (HEK) 293 cells, that express ANTXRs at undetectable levels. Furthermore, ectopic expression of ANTXRs in HEK293 cells did not affect the sensitivity to ATX treatment. These findings suggest that there is an ANTXR-independent cytotoxic mechanism in human cells.
几种动物模型已表明，炭疽毒素（ATX）通过炭疽毒素受体（ANTXR）功能对宿主细胞产生细胞毒性作用。在本研究中，与小鼠细胞相比，从人身上获取的细胞对ATX介导的细胞毒性表现出低敏感性，且该敏感性与ANTXRs的表达水平无关。ATX处理在其他培养的人细胞、人胚胎肾（HEK）293细胞中也诱导了细胞毒性作用，而这些细胞中ANTXRs的表达水平无法检测到。此外，在HEK293细胞中异位表达ANTXRs并不影响对ATX处理的敏感性。这些发现表明，在人细胞中存在一种不依赖于ANTXR的细胞毒性机制。
