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In addition, DAEC adhesion is accompanied by brush border lesion, F-actin
rearrangement and tight junction disruption (
Bernet-Camard et al., 1996
;
Pei-
ffer et al., 2000
). As a result of the adherence process, the bacteria become
firmly attached to the cell surface, initiating the colonization steps and acti-
vation of signal transduction pathways, resulting in the internalization of the
bacteria and/or inflammatory responses.
Internalization
A small proportion of adherent Afa/Dr DAEC strains are able to invade cul-
tured epithelial cells, a process that is also associated with the Afa/Dr adhesins
(
Guignot et al., 2009
). During in vitro culture, Afa/Dr DAEC invades epithelial
cells by a zipper-like mechanism, with the participation of microtubules, lipid
rafts and α5β1 integrins (
Goluszko et al., 1999
;
Kansau et al., 2004
;
Guignot
et al., 2009
). Once in the cytoplasm, internalized bacteria reside in a large vacu-
ole formed by the fusion of single bacterium-containing vacuoles originated
early during the initial step of invasion (
Plancon et al., 2003
;
Servin, 2005
).
Inlammation
DAEC infection is characterized by the induction of an inflammatory response
on epithelial cells. Afa/Dr DAEC infection of intestinal cultured cells induces
the release of pro-inflammatory factors, such as IL-8, as a result of the acti-
vation of the mitogen-activated protein kinases pathway (
Betis et al., 2003a
;
Arikawa et al., 2005
). The inflammation induced by Afa/Dr DAEC promotes
polymorphonuclear migration across the epithelial barrier, inducing the produc-
tion of TNF-α and IL-1β, which stimulate the production of DAEC receptor
DAF (
Betis et al., 2003b
). In addition, Afa/Dr DAEC increase the cell-surface
expression of the major histocompatibility complex class I chain-like gene A,
a key factor in the host innate immune response (
Tieng et al., 2002
). Overall,
these data provide a mechanism by which Afa/Dr DAEC may participate in the
development of inflammatory diarrhea in humans.
Clinical manifestations
Transmission and clinical features
Acquisition through food or water contaminated with human or animal feces
comprises the main transmission route for this pathovar. Clinical presentation
of diarrhea episodes caused by diarrhea-causing DAEC might include watery
or bloody diarrhea, abdominal cramps, dehydration and fever (
Gunzburg et al.,
1993
;
Jallat et al., 1993
); however, a unique clinical characteristic specific for
DAEC intestinal infection has not been described. Interestingly, the finding that
Afa/Dr DAEC adhesins are carried by
E. coli
causing UTIs supports the hypoth-
esis of fecal-perineal-urethral transmission as the etiology for these infections
(
Daigle et al., 1994
;
Foxman et al., 1995
).
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