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“Background Listeria monocytogenes is a Gram-positive, facultative learn more intracellular pathogen that can infect humans and animals after ingestion of contaminated food. It is responsible for human listeriosis, a disease predominantly affecting immunocompromised individuals. It can manifest 5-Fluoracil concentration itself in a wide range of clinical symptoms including meningitis or meningoencephalitis, gastroenteritis, abortion, perinatal infection, and septicemia [1, 2].

Central to the pathogenesis of listeriosis is the ability of the bacterium to cross host epithelial barriers. After oral infection L. monocytogenes can breach the intestinal barrier via invasion of intestinal epithelial cells or via transcytosis of goblet cells [3] or microfold

(M) cells in Peyer’s Patches [4, 5]. The pathogen is then able to spread systemically by the hematogenous and lymphatic route to internal organs. The ability of L. monocytogenes to cross the blood–brain and placental barriers to invade the central nervous system and the {Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|Selleckchem Anti-diabetic Compound Library|Selleckchem Antidiabetic Compound Library|Selleckchem Anti-diabetic Compound Library|Selleckchem Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|buy Anti-diabetic Compound Library|Anti-diabetic Compound Library ic50|Anti-diabetic Compound Library price|Anti-diabetic Compound Library cost|Anti-diabetic Compound Library solubility dmso|Anti-diabetic Compound Library purchase|Anti-diabetic Compound Library manufacturer|Anti-diabetic Compound Library research buy|Anti-diabetic Compound Library order|Anti-diabetic Compound Library mouse|Anti-diabetic Compound Library chemical structure|Anti-diabetic Compound Library mw|Anti-diabetic Compound Library molecular weight|Anti-diabetic Compound Library datasheet|Anti-diabetic Compound Library supplier|Anti-diabetic Compound Library in vitro|Anti-diabetic Compound Library cell line|Anti-diabetic Compound Library concentration|Anti-diabetic Compound Library nmr|Anti-diabetic Compound Library in vivo|Anti-diabetic Compound Library clinical trial|Anti-diabetic Compound Library cell assay|Anti-diabetic Compound Library screening|Anti-diabetic Compound Library high throughput|buy Antidiabetic Compound Library|Antidiabetic Compound Library ic50|Antidiabetic Compound Library price|Antidiabetic Compound Library cost|Antidiabetic Compound Library solubility dmso|Antidiabetic Compound Library purchase|Antidiabetic Compound Library manufacturer|Antidiabetic Compound Library research buy|Antidiabetic Compound Library order|Antidiabetic Compound Library chemical structure|Antidiabetic Compound Library datasheet|Antidiabetic Compound Library supplier|Antidiabetic Compound Library in vitro|Antidiabetic Compound Library cell line|Antidiabetic Compound Library concentration|Antidiabetic Compound Library clinical trial|Antidiabetic Compound Library cell assay|Antidiabetic Compound Library screening|Antidiabetic Compound Library high throughput|Anti-diabetic Compound high throughput screening| fetalplacental unit is associated with the most severe and often fatal forms of Listeria infections in immunocompromised patients and pregnant women [6]. Two bacterial surface proteins, Internalin A (InlA) and Internalin B (InlB) play a major role in the internalisation of L. monocytogenes into non-phagocytic cells and in the crossing of epithelial barriers [3, 7–9]. The molecular interaction

of both internalins with their respective receptors is species-specific. InlA induces listerial internalisation into intestinal Sinomenine epithelial cells by binding to the N-terminal domain of the human E-cadherin (Cdh1) cell adhesion protein [10]. It can also interact with Cdh1 from guinea pig, rabbit and gerbil but fails to bind to the corresponding domain of the murine and rat Cdh1. This species specificity is mostly determined by the presence of a proline at the 16th amino acid position of Cdh1 in permissive species and of a glutamic acid in non-permissive species [10–12]. InlB binds to the mouse, human, and gerbil Met receptor and can induce listerial uptake in a wide range of different mammalian cell types including hepatocytes and epithelial cells but cannot recognise the guinea pig and rabbit Met receptors [13, 14]. The species-specific receptor interactions of InlA and InlB have limited the development of small animal models to study mechanisms of L. monocytogenes dissemination and pathogenesis after oral infection. A major breakthrough was the generation of a transgenic mouse line which expresses the human E-cadherin (CDH1) gene under the control of the enterocyte specific promoter of intestinal fatty-acid-binding protein. This mouse model demonstrated for the first time that the interaction of InlA with Cdh1 is crucial for listerial intestinal invasion in vivo[15].