The induction of Infb1 www.selleckchem.com/products/Belinostat.html correlated with the systemic dissemination of Lmo-InlA-mur-lux bacteria from the intestine to internal organs as these were detected earlier by BLI analysis of the bacterial luciferase reporter gene in Lmo-InlA-mur-lux infected animals compared to Lmo-EGD-lux infected mice. In the present study we were not able

to detect differences in the Lmo-InlA-mur-lux and Lmo-EGD-lux invasion of the brain amongst the different mouse inbred strains investigated. Invasion of the CNS after oral infection with L. monocytogenes is still poorly understood despite the importance of Semaxanib neurological complications in fatal cases of listeriosis [33]. Different hypotheses for routes of listerial neuroinvasion have been suggested including a retrograde transport of the L. monocytogenes from the oral epithelium to the rhombencephalon in cranial nerves [64, 65] or dissemination of bacteria by the hematogenous route across the blood–brain barrier (BBB), either directly by extracellular bacteria in the blood [66] or via Selleckchem Mizoribine a Trojan horse mechanism by which intracellular bacteria are transported by infected leukocytes across the BBB [67–69]. Within the BBB, cells of the microvascular endothelium and the choroid plexus epithelium express both host receptors, Cdh1 and Met, for InlA and InlB, respectively [33].

Thus, theoretically these cells should be accessible for InlA- and InlB-mediated L. monocytogenes invasion. However, in our study we did not find any evidence for an InlA-dependent brain invasion mechanism. The occurrence

of neurolisteriosis as indicated by abnormal neurological behaviour of mice after oral infection with Lmo-InlA-mur-lux or Lmo-EGD-lux was an extremely rare event. From a total of 290 analysed animals, only three mice displayed ataxia or circling behaviour after infection. Two of these animals had been infected with Lmo-InlA-mur-lux and one mouse with Lmo-EGD-lux. All three affected animals Edoxaban were from different inbred mouse strains. Furthermore, our analysis of Lmo-InlA-mur-lux and Lmo-EGD-lux bacterial loads in the brain did not detect major differences between both listerial strains. Although, BALB/cJ mice did show higher bacterial loads for Lmo-InlA-mur-lux at 3 d.p.i. in the brain, they were not longer detectable by 5 and 7 d.p.i., and had no effect on the prevalence of neurological symptoms in this mouse strain. Therefore, we conclude that at least in our murinised L. monocytogenes infection model, InlA-Cdh1 interactions do not play a role in Listeria CNS neuroinvasion. By using a new, natural L. monocytogenes infection model which involved feeding of contaminated food to mice, Bou Ghanem and colleagues have very recently shown that InlA is not required for the initial establishment of intestinal infection in mice [70].