In vitro and in vivo models to study human listeriosis: mind the gap

Listeria monocytogenes (Lm) is the etiological agent of listeriosis, one of the deadliest human foodborne infections. Lm is able to cross the intestinal, placental and blood–brain barriers, leading to septicemia, fetoplacental infection, meningitis and encephalitis. The intracellular life cycle of this facultative intracellular bacterium has been studied in detail in in vitro cell culture systems. Lm enters in non-phagocytic cells in an InlA–Ecad and/or InB-Met dependent manner. Lm then escapes from its internalization vacuole via the action of the pore forming toxin LLO and spreads from cell to cell in an ActA-dependent manner. In vivo studies in “humanized” mouse models and human epidemiological data have led to the deciphering of the mechanisms underlying Lm crossing of intestinal and placental barriers. As illustrated in this review, in vivo outcomes could not be deduced directly from in vitro observations, and led to revisit the intracellular fate of Lm during infection.