Biology Reference
In-Depth Information
The expression, secretion, and translocation of effector proteins that enable the
bacteria to subvert host cellular pathways and cause disease are tightly regu-
lated. These virulence factors are regulated by elements encoded on the EAF
plasmid as well as the LEE pathogenicity island.
The EAF plasmid
The large (50-70 MDa) EAF plasmid harbored by tEPEC strains is required for
localized adherence (LA;
Figure 4.1
A) (
Baldini et al., 1983
;
Nataro et al., 1985
;
McConnell et al., 1989
). Curing the EAF plasmid from EPEC abolished LA and
autoaggregation phenotypes (
Figure 4.1
B) (
Baldini et al., 1983
;
Knutton et al.,
1987a
;
Chart et al., 1988
) and led to attentuated virulence in colostrum-deprived
piglets (
Baldini et al., 1983
) and healthy volunteers (
Levine et al., 1985
). How-
ever, plasmid-cured EPEC retained the ability to form A/E lesions (
Figure 4.1
C)
(
Baldini et al., 1983
;
Knutton et al., 1987a,b
;
Tzipori et al., 1989
) and transfer
of the EAF plasmid to non-EPEC strains endowed them with the ability to carry
out LA (
Baldini et al., 1983
;
Knutton et al., 1987b
).
Sequence analysis of the EAF plasmid from E2348/69, pMAR7, a modified
pMAR2 plasmid that carries an ampicillin resistance marker, revealed it to be a
(A)
(B)
(C)
(D)
FIGURE 4.1
EPEC phenotypes: (A) Localized adherence (LA) of EPEC to HEp-2 epithelial cells
in tissue culture. Arrow indicates a representative microcolony of EPEC. (B) Autoaggregation of
EPEC in DMEM tissue culture medium. Portions of two aggregates are shown. (C) Attaching and
effacing (A/E) of T84 cells by EPEC. The arrow indicates a site of intimate adherence between a
bacterium and host cell (courtesy of Barry McNamara). (D) Fluorescent-actin staining (FAS) of
EPEC adhering to HeLa cells. FITC-labeled phalloidin was used to identify highly concentrated
actin filaments localizing beneath EPEC.
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