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intestinal epithelial cells with a macropinocytosis-like entry process; (ii) ability to
survive and replicate within macrophages without triggering host cell death; and
(iii) ability to induce the release of large amounts of TNF-α from infected macro-
phages (
Darfeuille-Michaud, 2002
;
Darfeuille-Michaud et al., 2004
).
History
In 1932, Dr. Burrill B. Crohn and colleagues presented a paper to the Ameri-
can Gastro-Enterological Association entitled 'Non-specific Granulomata of the
Intestine', describing the features of what is now known as CD, a disease different
from UC (
Baron, 2000
;
Naser et al., 2012
). It was speculated that an infectious
agent could account for an environmental cause of the disease. In 1970, Rees and
Mitchel showed that mice inoculated with CD tissue displayed focal granulomas
(
Mitchell and Rees, 1970
). Subsequently, Cave and collaborators demonstrated
that rabbits inoculated with human CD tissue homogenates developed granuloma
(
Cave et al., 1973
) and this effect could be prevented by ampicillin pretreatment
of the homogenates (
Donnelly et al., 1977
), suggesting the presence of a trans-
missible agent in the disease. Other studies showed that antibody titers against
E. coli
antigens were higher in CD patients than in controls (
Brown and Lee,
1973
;
Tabaqchali et al., 1978
) and that most CD tissue samples were positively
labeled by anti-
E. coli
antibodies (
Cartun et al., 1993
;
Liu et al., 1995
).
E. coli
were
recovered frequently from CD tissues (
Darfeuille-Michaud et al., 1998
), and these
isolates were shown to be genetically related by their ribotype profiles (
Masseret
et al., 2001
), and able to adhere to differentiated intestinal epithelial cells more
frequently than isolates from healthy tissues (
Darfeuille-Michaud et al., 1998
;
Masseret et al., 2001
). Additionally, the reference AIEC LF82 strain was shown to
invade and replicate inside intestinal epithelial cells, using a process dependent on
a macropinocytosis-like mechanism (
Darfeuille-Michaud, 2002
). Based on those
characteristics, the designation of adherent-invasive
E. coli
as a new group of
E. coli
associated with CD was proposed (
Darfeuille-Michaud, 2002
).
Evolution
The onset and perpetuation of CD has not been associated with any particular
E. coli
strain, but the use of culture-independent methods of identification sug-
gested that most
E. coli
strains colonizing CD lesions are genetically related. Ribo-
typing of
E. coli
isolates from CD patients with early, recurrent, or chronic lesions,
with or without endoscopic recurrence showed that, while compared to healthy
controls, most
E. coli
from CD cases grouped in a single ribotype profile (
Masseret
et al., 2001
).
E. coli
species comprises four phylogenetic groups: A, B1, B2, and D,
and the CD-specific isolates were found to belong to B2 and D groups (
Kotlowski
et al., 2007
). A recent study did not find any phylogenetic relationship among
CD
E. coli
isolates and most of the phylogenetic groups were found equally dis-
tributed in CD patients and healthy individuals; however, the B2 phylogroup was
more prevalent among AIEC-positive isolates (
Martinez-Medina et al., 2009
).
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