p.i. with higher loads of murinised Lmo-InlA-mur-lux bacteria, these differences were not further detectable at 5 and 7 days p.i.. We therefore conclude that at least in our infection system, InlA-Cdh1 Veliparib order interactions do not play a role in the dissemination of L. monocytogenes to the brain. Moreover, even in different mouse genetic backgrounds no evidence for InlA-mediated CNS infection was found. Table 1 Neurological symptoms in mouse inbred strains after oral infection with Lmo-InlA-mur-lux and

Lmo-EGD-lux L. monocytogenes strain Mouse inbred strain Total number of mice infected Number of mice displaying neurological abnormalities Symptoms occurrence time post infection [days] Lmo-InlA-mur-lux C3HeB/FeJ 40 0     A/J OlaHsd 30 1 7   BALB/cJ 30 0     C57BL/6J 30 1 7     ∑ 130 ∑ 2   Lmo-EGD-lux C3HeB/FeJ 40 0     A/J OlaHsd 40 0     BALB/cJ 40 1 7   C57BL/6J RGFP966 order 40 0       ∑ 160 ∑ 1   Discussion In vivo bioluminescence imaging is an important technology for the spatial-temporal monitoring of infection processes that underlie microbial pathogenesis and host defence mechanisms [30, 36]. Importantly, BLI allows repeated non-invasive imaging of pathogen dissemination to target organs and was used to identify the murine gallbladder as a novel

organ of infection and as a host reservoir for extracellular Listeria replication and pathogen shedding [19, 37]. In the present study, we have combined an InlA and Anidulafungin (LY303366) InlB permissive mouse infection model of L. monocytogenes[12] with BLI, bacterial growth, and histopathology. We accurately compared resistance of mouse strains of different genetic backgrounds to orally acquired murinised and non-murinised Listeria. We identified the C3HeB/FeJ, A/J, and BALB/cJ strains as being susceptible to oral L. monocytogenes challenge whereas C57BL/6J mice were resistant. BLI analysis was more sensitive than bacterial culture or histopathology at detecting differences in pathogenesis between the murinised and non-murinised Listeria strains, and demonstrated that in the susceptible mouse inbred

strains Lmo-InlA-mur-lux spread to internal organs more quickly and in higher APR-246 numbers when compared to Lmo-EGD-lux infected animals. Thus, murinised Listeria can efficiently be used with mice of different genetic backgrounds for studies on mechanisms of orally acquired listeriosis. Importantly, once the intestinal barrier has been overcome by the pathogen, patterns of L. monocytogenes host resistance that have been previously determined by using systemic infection models are very similar to those that were observed in our present study. C57BL/6J mice are resistant to both oral and intravenous L. monocytogenes infection challenge, whereas C3HeB/FeJ, A/J and BALB/cJ mice are highly susceptible in both mouse infection models [38–42]. We show here that the host resistance of C57BL/6J mice to intragastric L.