Perforin-2 (MPEG1) knockout mice are not resistant to LPS induced septic shock.

In this animal model LPS is injected to induce sterile septic shock. C57BL/6 and 129X1/SvJ wild-type and perforin-2 (mpeg1) knockout mice were injected intraperitoneally with LPS from <i>E. coli</i> 0111:B4 (InvivoGen LPS-EB ultra-pure, catalog # tlrl-3pelps). Mice were monitored hourly for signs of morbidity and humanely euthanized as per IACUUC protocol. "1" indicates subject death, "0" indicates censored subject. On either genetic background the differences between survival rates of WT and perforin-2 KO animals are insignificant. Crucially, we did observe that 129 mice were more resistant to LPS challenge than BL6 mice. This was expected due to the caspase 11 mutation carried by 129s. <i>All animal experiments were approved by and performed in accordance with the University of Miami Institutional Animal Care and Use Committee guidelines.</i><i><br></i><b>Experiment 1. </b>LPS challenge of WT and perforin-2 (mpeg1) -/- C57BL/6 and 129X1/SvJ mice<br><b>Experiment 2</b>. LPS challenge of WT and perforin-2 (mpeg1) -/- 129X1/SvJ mice本动物模型采用脂多糖（LPS）注射诱导无菌性脓毒症休克。实验选用C57BL/6与129X1/SvJ两种品系的野生型（WT）及穿孔素2（mpeg1）敲除（KO）小鼠，经腹腔注射给予大肠杆菌（*E. coli*）0111:B4来源的超纯LPS-EB（InvivoGen公司，货号tlrl-3pelps）。每小时监测小鼠发病体征，并按照实验动物管理与使用委员会（IACUC）规程对小鼠实施安乐死。以“1”表示受试动物死亡，“0”表示截尾受试动物。在两种遗传背景下，野生型与穿孔素2敲除小鼠的生存率差异均无统计学意义。值得注意的是，本研究观察到129系小鼠对LPS攻击的耐受性显著高于BL6系小鼠，这一结果符合预期，因129系小鼠携带半胱天冬酶11（caspase 11）突变。*所有动物实验均经迈阿密大学实验动物管理与使用委员会批准，并严格遵循其指南开展。* **实验1：** 大肠杆菌（*E. coli*）0111:B4来源LPS攻击野生型与穿孔素2（mpeg1）敲除C57BL/6及129X1/SvJ小鼠 **实验2：** 大肠杆菌（*E. coli*）0111:B4来源LPS攻击野生型与穿孔素2（mpeg1）敲除129X1/SvJ小鼠