中文摘要：

为研究sopE2基因对肠炎沙门菌（Salm onella enteritidis）的生物学特性的影响及其与sopE功能差异,本研究以λ-Red介导的同源重组法构建了肠炎沙门菌C50336ΔsopE2缺失株,并构建了以pBR322质粒介导的sopE2基因回复株。测定了肠炎沙门菌野生株、sopE2缺失株及其回复株的基本生物学特性,包括对人肠上皮细胞Caco-2 BBE及小鼠巨噬细胞RAW 264.7的黏附、侵袭能力及对小鼠的半数致死量。结果显示,肠炎沙门菌sopE2基因缺失对其生长、生化特性无影响;肠炎沙门菌C50336对Caco-2 BBE细胞的黏附率约为20%,侵袭率约为10%,对RAW264.7细胞的黏附率约为55%,侵袭率约为20%,sopE2基因缺失对肠炎沙门菌C50336黏附能力无影响,侵袭能力有所下降,但无统计学差异;肠炎沙门菌C50336对小鼠的半数致死量为5.0×10^5CFU,sopE2基因缺失株及回复株对小鼠的半数致死量均为3.2×10^5CFU,表明sopE2基因缺失对肠炎沙门菌的毒力无显著影响。本研究为进一步探讨sopE2基因在肠炎沙门菌感染过程中的功能奠定了基础。

英文摘要：

To investigate the role of a sopE2 gene from Salmonella enteritidis in biological characteristics and reveal the functional difference between sopE2 and sopE effector,we deleted the sop E2 gene in Salmonella enteritidis strain C50336 using λ-Red recombinant system,and obtained a complementary strain by transforming plasmid p BR322-sop E2 into the mutant strain.The biological characteristics including growth property,biochemical property,ability of adhesion and invasion to human epithelial cells Caco-2 BBE and mouse macrophage RAW264.7,and median lethal dose（LD50） for mouse were then compared among the three strains.Our results showed that there was no obvious difference in growth property and biochemical properties among those three strains.The in-vitro infection analysis showed that no significant difference was detected in the adhesion and invasion ability among those stains.For Caco-2 BBE cells,the adhesion and invasion rate was approximately 20% and 10%,respectively.But for RAW264.7 cells,the adhesion and invasion rate reached approximately 55% and 20%,respectively.Furthermore,the study of LD50 revealed that deletion of sopE2 did not cause the decreased virulence to mouse.The above-mentioned results provides the foundation for studying the role of sop E 2 in the process of Salmonella enteritidis infection.