Listeria monocytogenes causes
listeriosis, a human
foodborne infection leading to
gastroenteritis,
meningoencephalitis and maternofetal
infections. InlA and InlB, two
L. monocytogenes surface proteins, interact with their respective receptors
E-cadherin and Met and mediate
bacterial entry into human cultured cells. Here, we present protocols for studying
listeriosis in three complementary animal models: (i) the human
E-cadherin (hEcad)
transgenic mouse line; (ii) the
knock-in E16P
mouse line; and (iii) the gerbil, in which both InlA-E-cadherin and InlB-Met species-specific interactions occur as in humans. Two
routes of infection are described: oral
inoculation, the natural route for
infection; and
intravenous inoculation that bypasses the
intestinal barrier. We describe how to monitor
L. monocytogenes infection, both qualitatively by imaging techniques and quantitatively by
bacterial enumeration. The advantage of these methods over the classical
intravenous inoculation of
L. monocytogenes in
wild-type mice (in which the InlA-E-cadherin interaction does not occur) is that it allows the
pathophysiology of
listeriosis to be studied in animal models relevant to humans, as they are
permissive to the interactions that are thought to mediate
L. monocytogenes crossing of human host barriers. The whole procedure (
inoculation, in vivo imaging,
bacterial enumeration,
histopathology) takes one full week to complete, including 3 d of actual experiments.
