Genetic control in the susceptibility of germfree inbred mice to infection by Escherichia coli O115a,c:K(B).
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.
Itoh
K
K
Animal and Cellular Systems Laboratory, Institute of Physical and Chemical Research, Saitama, Japan.
Matsui
T
T
Tsuji
K
K
Mitsuoka
T
T
Ueda
K
K
D000818:Animals; D002432:Cecum / Q000473:pathology; D004751:Enteritis / Q000235:genetics* / Q000473:pathology; D004926:Escherichia coli / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000235:genetics*; D005243:Feces / Q000382:microbiology; D005856:Germ-Free Life; D007420:Intestine, Large / Q000382:microbiology; D051379:Mice; D008815:Mice, Inbred Strains / Q000502:physiology