Donnenberg M S, Tacket C O, James S P, Losonsky G, Nataro J P, Wasserman S S, Kaper J B, Levine M M
Center for Vaccine Development, University of Maryland, Baltimore 21201.
J Clin Invest. 1993 Sep;92(3):1412-7. doi: 10.1172/JCI116717.
Enteropathogenic Escherichia coli (EPEC) infections are a leading cause of infant diarrhea in developing countries. Recently eaeA, a gene necessary for the characteristic intimate attachment of EPEC to epithelial cells in tissue culture, was described. We conducted a randomized, double-blind study to determine the role of the eaeA gene in human EPEC infection. 11 adult volunteers ingested 2 x 10(10) colony-forming units of O127:H6 EPEC strain E2348/69, and an equal number received the same dose of an isogenic eaeA deletion mutant constructed from E2348/69. Volunteers were monitored for the development of diarrhea, fever, and systemic and gastrointestinal complaints. Diarrhea developed in all 11 volunteers who received E2348/69 and in 4 of 11 who received the mutant (P = 0.002). Fever was more common in recipients of the wild-type strain (P = 0.024). Stool volumes were lower in recipients of the mutant. All volunteers seroconverted to E2348/69 LPS, but the geometric mean peak titers of serum IgG and IgA in recipients of the mutant were lower than those of recipients of the wild-type strain. IgA against LPS was detected in the jejunal fluid of six of six recipients of E2348/69 and 5/6 recipients of the mutant. This study unambiguously assigns a role for eaeA as an EPEC virulence gene, but the residual diarrhea seen in recipients of the mutant indicates that other factors are involved.
肠致病性大肠杆菌(EPEC)感染是发展中国家婴儿腹泻的主要原因。最近,人们发现了eaeA基因,它是EPEC在组织培养中与上皮细胞紧密附着所必需的基因。我们进行了一项随机双盲研究,以确定eaeA基因在人类EPEC感染中的作用。11名成年志愿者摄入了2×10¹⁰个菌落形成单位的O127:H6 EPEC菌株E2348/69,同样数量的另一组志愿者接受了相同剂量的由E2348/69构建的同基因eaeA缺失突变体。对志愿者进行腹泻、发热以及全身和胃肠道不适症状的监测。接受E2348/69的11名志愿者均出现腹泻,而接受突变体的11名志愿者中有4人出现腹泻(P = 0.002)。野生型菌株接受者发热更为常见(P = 0.024)。突变体接受者的粪便量较少。所有志愿者的血清都转化为对E2348/69脂多糖(LPS)呈阳性反应,但突变体接受者血清IgG和IgA的几何平均峰值滴度低于野生型菌株接受者。在接受E2348/69的6名志愿者和接受突变体的5/6志愿者的空肠液中检测到了抗LPS的IgA。这项研究明确了eaeA作为EPEC毒力基因的作用,但在突变体接受者中观察到的残留腹泻表明还有其他因素参与其中。