It has been established that

LLS plays a role in the survival of L. monocytogenes in PMNs and also contributes to virulence in the murine model [8]. LIPI-3 consists of 8 genes arranged in the following order: llsAGHXBYDP. LlsA is the structural peptide; LlsB, Y and D are enzymes proposed to perform the post-translational modifications; LlsGH is an ABC transporter; LlsP is a protease; while LlsX is of unknown function [7, 8]. The associated promoter, PllsA, which is situated upstream of llsA, is not transcribed in standard laboratory media but is induced by oxidative stress. It has been suggested that expression of the LIPI-3 genes may be induced in the phagosome of macrophages [8]. When PllsA is replaced selleck chemical by a constitutive

promoter (PHELP), a strongly haemolytic/cytolytic phenotype is revealed {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| under laboratory conditions [8]. The inducible nature of LLS and its absence in many L. monocyctogenes strains is probably responsible for the fact that this virulence factor has gone undetected until recently. Listeria innocua is an avirulent species within the Genus Listeria. It has been proposed that L. innocua and L. monocytogenes have evolved from a common ancestor and differ predominantly due to the loss of virulence genes by L. innocua[10, 11]. This is supported by the existence of atypical L. innocua isolates which retain LIPI-1 and other virulence factors [12, 13]. In a previous investigation we demonstrated that none of 11 L. innocua isolates examined (one of which was initially classified as an L. grayi isolate) possessed the equivalent of the LIPI-3

[7, 8]. In this study we extended our analysis to a larger collection of strains, which has revealed that several strains possess the remnants of a LIPI-3. In fact, 11 strains possess fully intact LIPI-3 which gives rise to a haemolytic phenotype when the genes are constitutively expressed. Methods Strains and growth conditions Tables  1, 2, and 3 list the panel of Listeria strains used in this study. Strains were obtained from the Food Microbiology Microbial Collection (University College Cork) and the Special Listeria Sinomenine Culture Collection (SLCC). All strains were cultured at 37°C for 16 h in Brain Heart Infusion (BHI) broth or agar (Oxoid, Hampshire, UK) unless otherwise stated. Where necessary, the characterisation of strains as L. innocua was confirmed biochemically by means of the API listeria kit (BioMérieux, Lyon, France) and 16S ribosomal DNA (rDNA) with CO1 and CO2 primer pairs previously described by Simpson et al.[14]. Escherichia coli EC101 was used as an intermediate vector host. Antibiotics were GANT61 solubility dmso incorporated as follows [8]: Erythromycin (Ery) 150 μg/ml E. coli, 5 μg/ml L. innocua.