Abstract
Enteropathogenic Escherichia coli (EPEC) O111:H2, O119:H6, or O142:H6 caused rapid detachment of Chinese hamster ovary (CHO) cell monolayers within 2 to 4 h of cocultivation. CHO cell detachment was not promoted by nonenteropathogenic E. coli (O125:H4, O126:H27, O157:H7, and O26:H11) and could not be attributed to EPEC production of enterohemolysin or Shiga-like toxins. In contrast, EPEC strains did not promote rapid detachment of Lec1, Lec2, or Lec8 CHO cell monolayers. These CHO cell Lec mutants all express abbreviated glycan sequences on membrane glycoproteins and glycolipids. Although EPEC strains failed to alter the adherent properties of Lec2 cells lacking only terminal sialic acid groups, EPEC adherence to the Lec2 mutant was indistinguishable from that observed with wild-type CHO cells. There was also no significant difference in EPEC-induced actin accumulation or invasion of Lec2 cells. In contrast, EPEC localized adherence to Lec1 and Lec8 mutants, lacking sialyllactosamine (Lec1) or sialic acid and galactose (Lec8) sequences, was reduced by 84 and 93%, respectively. Our results suggest that lactosamine sequences [beta Gal(1-4 or 1-3)beta GlcNAc] not containing sialic acid are sufficient for EPEC adherence, actin accumulation, and invasion of CHO cells. Sialic acid groups, however, may be necessary for EPEC-mediated CHO cell detachment.
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