Itoh K, Matsui T, Tsuji K, Mitsuoka T, Ueda K
Animal and Cellular Systems Laboratory, Institute of Physical and Chemical Research, Saitama, Japan.
Infect Immun. 1988 Apr;56(4):930-5. doi: 10.1128/iai.56.4.930-935.1988.
We studied the susceptibility of five germfree inbred strains of mice to oral infection by murine pathogenic Escherichia coli O115a,c:K(B) (MPEC), the causative agent of mouse megaenteron. Although MPEC colonized all strains of mice at 10(9)/g of feces, the mouse strains could be divided into three groups according to their intestinal lesions. In CF1 and C3H/He mice, intestinal lesions were produced in the cecum and colon with hyperplasia of epithelial cells accompanied by severe inflammatory reactions and erosion. The lesions in NC and C57BL/6 mice were restricted to the tip of the cecum, and hyperplasia of epithelial cells was more severe in these mice than in CF1 or C3H/He mice. BALB/c mice had no lesions. Analysis of F1 hybrids of CF1, NC, and BALB/c mice and offsprings from backcrosses of F1 mice to parental strains showed that susceptibility to MPEC seemed to be controlled genetically by a single locus which may be related to the receptors on epithelial cells for MPEC adherence. However, the differences in lesions between CF1 and NC mice suggest that a combination of this locus and another locus to which it may be related regulates the hyperplasia of intestinal epithelial cells.
我们研究了五种无菌近交系小鼠对小鼠致病性大肠杆菌O115a,c:K(B)（MPEC，小鼠巨肠症的病原体）口服感染的易感性。尽管MPEC在所有小鼠品系的粪便中定殖量均达到10⁹/g，但根据肠道病变情况，这些小鼠品系可分为三组。在CF1和C3H/He小鼠中，盲肠和结肠出现肠道病变，伴有上皮细胞增生，并伴有严重炎症反应和糜烂。NC和C57BL/6小鼠的病变局限于盲肠尖端，且这些小鼠上皮细胞的增生比CF1或C3H/He小鼠更为严重。BALB/c小鼠没有病变。对CF1、NC和BALB/c小鼠的F1杂种以及F1小鼠与亲本品系回交后代的分析表明，对MPEC的易感性似乎由一个单一位点进行遗传控制，该位点可能与MPEC黏附的上皮细胞受体有关。然而，CF1和NC小鼠之间病变的差异表明，该位点与另一个可能相关的位点共同作用调节肠道上皮细胞的增生。
