PubMedCrossRef 39. Shaw DM, Gaerthé B, Leer RJ, Van der Stap JG, Smittenaar C, Heijne Den Bak-Glashouwer M, Thole JR, Tielen FJ, Pouwels PH, Havenith CE: Engineering the microflora to vaccinate the mucosa: serum immunoglobulin G responses and activated draining cervical lymph nodes following mucosal application of tetanus toxin fragment C-expressing lactobacilli . Immunology 2000, 100:510–518.PubMedCrossRef 40. Xin KQ, Hoshino Y, Toda Y, Igimi S, Kojima Y, Jounai

N, Ohba K, Kushiro A, Kiwaki M, Hamajima K, Klinman D, Okuda K: Immunogenicity and protective efficacy of orally administered recombinant Lactococcus lactis expressing surface-bound HIV. Env Blood 2003, 102:223–228.CrossRef 41. Fagarasan S, Honjo T: Intestinal IgA synthesis: regulation of front-line body defences. Nat Rev Immunol 2003, 3:63–72.PubMedCrossRef 42. Sambrook J, Fritisch EF, Maniatis T: Molecular Cloning: A Laboratory Manual. 3 Edition New York: Cold Spring Harbor Laboratory GDC-941 2001. 43. Sambrook J, Fritisch EF, Maniatis T: Molecular cloning: a laboratory manual. 2 Edition Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY 1989. 44. Shifang J, Yinyu W, Xinhua G, Liandong H: The factors affected Mizoribine datasheet transformation efficiency of Lactobacillus by electroporation. selleck screening library Chin J Biotechnol 1998, 14:429–33. 45. Cortes-Perez NG, Luis G: Mice immunization with live lactococci displaying a surface anchored HPV-16 E7 oncoprotein. FEMS Microbiol Lett 2003, 229:37–42.PubMedCrossRef

46. McCluskie MJ, Davis HL: CpG DNA is a potent enhancer of systemic and mucosal immune responses against hepatitis B surface antigen with intranasal administration to mice. J Immunol 1998, 161:4463–4466.PubMed 47. Ho PS, Wang JK, Lee YK: Intragastric administration of Lactobacillus

casei expressing transmissible gastroentritis coronavirus spike glycoprotein induced specific antibody production. Vaccine 2005, 23:1335–42.PubMedCrossRef Authors’ contributions XQ carried out construction of expression plasmid, participated in the sequence alignment and drafted the manuscript. GL carried out the protein expression and immunoassays. XW and XL carried out the Immunizations. ML performed the statistical Montelukast Sodium analysis. YL conceived of the study, and participated in its design and coordination. All authors read and approved the final manuscript.”
“Background The Atlantic cod (Gadus morhua) is a cold-adapted fish species which has been captured for human consumption for many years. It is a perishable commodity and for that reason, preservation methods like freezing or salting have traditionally been used to extend its shelf life [1, 2]. The fish is a microbial ecosystem of its own where the ecological principles of succession are as valid as in any other ecosystem. This microbiological environment consists of a high nutrient content with an oxygen tension favourable to the proliferation of fast-growing heterotrophs also responsible for the spoilage of food [3–5].

High resolution microscopy (SEM, AFM), epifluorescence microscopy, lipid biomarkers’ analysis, 16sRNA analysis of isolated strains and routine microbiological techniques were applied. Living prokaryotic and eukaryotic microorganisms were observed in all samples investigated. The total cell’s amount in AntDinaciclib chemical structure Arctic and Arctic samples ranged to 107–108cells per gram dry weight and for most of them significantly exceeded CFU number (102–106). Among isolated strains from Antarctic permafrost were the representatives of gram positive bacteria Bacillus, Rhodococcus and gram negative bacteria Aureobacterium (Curtobacterium), or Comamonas Selleck Danusertib (Aquaspirillum). For

ancient Arctic ground ice among the dominants were gram positive strains of genera Arthrobacter, Promicromonospora and strains of gram negative bacteria of genera Flavobacterium. All isolated strains revealed the possibility to growth at wide range of temperatures. More than half of isolated bacterial strains were resistant to various antibiotics. Study of antibiotic resistance spectrum of all isolated from Arctic and Antarctic sediments strains showed not only single resistance to certain antibiotic, but also double resistance to various antibiotics. As revealed by method of 16sRNA analysis, among these strains were bacteria

of genera Acinetobacter, Paenibacillus and Brevundimonas It was revealed that endogenic physiological transformations of bacterial cells in permafrost sediments doesn’t depend on the lithogenesis, but to a grater extent on long persistence of temperature/or water availability. It could be expected, that in conditions of prolonged Epacadostat solubility dmso cell multiplication braking, the adaptive mutations proceed in microbial cells, increasing the vitally important potential of microorganisms. The obtained results provide new arguments to the whys and wherefores of the astrobiology search Chloroambucil of life on other planets with dominated subzero temperatures

(Mars). E-mail: second_​ks@mail.​ru Pyrolysis GC/MS Technique Application to Exobiology Yeghis Keheyan ISMN-CNR, c/o Dept. of Chemistry, University “La Sapienza”, p.le Aldo Moro 5, Rome-0185, Italy Many extraterrestrial objects are known to contain organic mater in the form of complex macromolecular materials. Pyrolysis coupled with gas chromatography and mass spectrometry (Py-GC–MS) is known to be powerful tool in analysing such materials and has been applied to the study of different complex organic matter contained in meteorites and interplanetary dust particles. The results of pyrolysis experiments to estimate survivability of different compounds of exobiological interest in oxygen-free (He) atmosphere will be reported. E-mail: yeghis.​keheyan@uniroma1.​it Early Survival, Pigment Spectra, and Productivity of Photosynthesis on M Star Planets Nancy Y. Kiang1,10, Antígona Segura2,10, Giovanna Tinetti3,10, Govindjee4, Robert E.

8 ± 5.7% increase in death of Jurkat cells. These

results suggest that the S20-3 peptide derived from the HHV-8 K1 protein selectively induces cell death in malignant hematological cells, but is not toxic to normal human cells. The S20-3 peptide kills cells in the absence of the Fas receptor To investigate whether S20-3–induced apoptosis depends on the signaling of the Fas receptor, we tested the S20-3 peptide in Fas-resistant see more Jurkat cell lines I2.1 and I9.2, which have defective FADD and caspase-8 functions, respectively [18]. The S20-3 peptide induced slightly less cell death in I2.1 cells than in the wild type ABT-263 in vivo Jurkat cells (21% vs. 24% above control; Figure 3A). The response of caspase-8 function-defective

Jurkat cell line I9.2 to the S20-3 peptide was significantly blunted compared with that of check details wild-type Jurkat cells (14.4% vs. 24% above control; 60% reduction) but not completely eliminated (Figure 3A). In line with this result, we found that the pan-caspase inhibitor z-VAD also only partially blocked S20-3-induced death in BJAB cells (8.9% vs. 13.3% above control; 67% reduction) (Figure 3B) as well as apoptosis induced by the Fas-agonistic antibody CH-11 (14% vs. 29% above control; 48% reduction) (data not shown). Figure 3 The S20-3 peptide–induced cell death is only partially dependent on caspases and involves necroptosis. (A) Jurkat (wild-type), Jurkat I9.2 Benzatropine (caspase-8–deficient), and Jurkat I2.1 (FADD-dominant-negative mutant) cell lines were incubated with 100 μM peptide S20-3. (B) BJAB cells were incubated with 100 μM peptide S20-3 in the presence or absence of 20 μM pan-caspase inhibitor z-VAD-FMK. (C) Daudi cells were incubated with 100 μM peptide S20-3 or buffer in the presence or absence of 20 μM pan-caspase inhibitor z-VAD-FMK. After 1 hour of incubation, cells were washed and incubated in complete medium

for 24 hours before flow cytometry analysis. Data in (A) and (B) are shown as means ± SD of triplicate wells; *P < 0.01. Further examination of the cell death induced by the S20-3 peptide in Daudi cells revealed that the S20-3 peptide induced necrosis (33.7% PI–positive cells) rather than apoptosis (0.3% AnnexinV–positive/PI–negative cells) in Fas-resistant Daudi cells (Figure 3C and Additional file 1: Figure S3A), and z-VAD further enhanced this effect (41.1% PI–positive cells) (Figure 3C). An LDH release assay further confirmed that the S20-3 peptide was causing necrosis as early as 1 hour post treatment (Additional file 1: Figure S3B).

Even a small volume of contrast may induce CIN in patients with severe kidney dysfunction. Physicians must determine the volume of contrast media to be used during contrast-enhanced

CT after careful consideration of the risks associated with the use of contrast media and the benefits of the examination. Patients with kidney dysfunction should undergo appropriate preventive procedures such as fluid therapy before and after contrast-enhanced CT, and should be closely followed up for kidney function and clinical condition. According to the formula described by Nyman et al. [94], the volumes of contrast media that are associated with the 5, 10, 20, and 30 % incidences of CIN in patients with different eGFRs can be calculated (Fig. 3). This formula has been validated in only 1 GSK2879552 order study by

the same researchers [52], and there is no sufficient evidence supporting the formula. Readers should be aware of this, Compound Library solubility dmso and should use these data only as a reference. Fig. 3 Volumes of contrast media associated with the 5, 10, 20 and 30 % incidences of CIN. (1) CIN was defined as an increase in SCr level by 44.2 mmol/L (0.5 mg/dL) or ≥20–25 % within 48–72 h after contrast exposure. (2) The formula used to calculate volume of contrast media associated with CIN has been validated in only 1 study by Nyman et al. [52], and there is no sufficient evidence supporting the formula. Readers should be aware of this, and should use these data only as a reference. The formula was developed on the basis of data of patients undergoing cardiac catheterization rather than CT. CIN contrast-induced nephropathy, CT computed tomography, eGFR estimated glomerular filtration rate, SCr serum contrast Quinapyramine media of 370 mg iodine/mL creatinine Does repeated contrast-enhanced CT at short intervals increase the risk for developing

CIN? Answer: We consider not to repeat contrast-enhanced CT within 24–48 h because repeated contrast-enhanced CT at short intervals may increase the risk for developing CIN. Patients with emergent conditions, such as those with ruptured cerebral aneurysm or acute myocardial infarction, may receive contrast media repeatedly within 24–48 h for the purposes of pre- and post-treatment assessment and MK 8931 intervention, among others. In a study of 164 patients who underwent repeated contrast-enhanced CT examinations within 24 h, 21 patients (12.8 %) developed CIN [96]. Because the incidence of CIN was higher than that reported in other studies of patients after single contrast-enhanced CT examination, it is possible that repeated contrast-enhanced CT may increase the incidence of CIN. In a study of 28 patients who underwent two contrast exposures, SCr levels increased and eGFR decreased statistically significantly after the second contrast exposure, and 4 of the 28 patients developed CIN [97].

The supplements were prepared in powder form and packaged in coded generic containers for double-blind administration

by an independent company (Command Nutritionals, Fairfield, NJ). Compliance to the supplementation protocol was monitored Anlotinib mw by a research nurse/dietician who contacted the study subjects on a weekly basis by telephone. Subjects were required to bring in their supplement bottles on workout days at weeks 3, 6 and 9 for DihydrotestosteroneDHT datasheet visual inspection by study personnel to assess compliance with the protocol. Side Effect Assessment A questionnaire was completed at weeks 3, 6 and 9 (workout sessions 12, 24 and 36) to monitor individual changes in DOMS and assess potential adverse events and change in sleep habits, general attitude, irritability, appetite, thirst, muscle soreness, muscle cramping, stomach distress, and headache, as well as any other idiosyncratic responses to the supplementation/training protocol. If identified, events were recorded as adverse events. In addition, subjects were contacted on a weekly basis by phone contact to inquire if they had experienced any find more adverse events, and were told to call at any time during the study to report side effects. Dietary (Nutrition) Monitoring The research dietitian met with each subject to explain the proper procedures for recording dietary intake. Each subject’s baseline diet (3-days: two weekdays & one

weekend day) was analyzed using the NutraBase IV Clinical Edition, (CyberSoft, Inc., Phoenix, AZ) to determine its energy and macronutrient content. Additional 3-day diet records were analyzed at weeks 3, 6 and 9 to verify that eating habits had remained consistent throughout the study. Resistance Training Protocol All subjects followed a specific 4-day per week workout designed by a Certified Strength and Conditioning Specialist (CSCS). The workout involved training the upper and lower body twice per week using a 4-day split (i.e., upper body1, lower body1, upper body2, lower body2) with gradual increases in volume and intensity. The workout consisted of at least 12 exercises,

including but not limited to: bench press, lat pulldown, shoulder press, seated row, shoulder shrug, dip, biceps curl, triceps push down, leg press, Smoothened squat, deadlift, lunge, leg curl, leg extension, and calf raise. For each exercise, subjects performed 3-6 sets of 8-15 repetitions with as much weight as they could handle with good form (typically 70-85% of the 1-repetition maximum). As subject strength and endurance improved, training resistances were progressively increased to maintain the required repetition range. Rest periods between exercises were 1-3 minutes, and between sets were 60-120 seconds. Training was conducted at the subject’s local training facility, documented in training logs, and signed off by fitness instructors/gym personnel to verify compliance. Two different facilities were utilized and identical equipment was available at both facilities.

World J Microbiol Biotechnol 2008, 24:1573–1577.CrossRef 24. Gotelli NJ, Entsminger GL: EcoSim: Null models software for ecology. Version 5.0. [http://​homepages.​together.​net/​~gentsmin/​ecosim.​htm] Acquired Intelligence Inc. & Kesey-Bear; 2000. 25. Apajalahti j: Comparative gut microflora, metabolic challenges, and potential opportunities. J Appl Poult Res 2005, 14:444–453. 26. Sobieszczańska

BM: Distribution of genes encoding iron uptake systems among enteroaggregative Escherichia coli strains isolated from adults with irritable bowel syndrome. Clin Microbiol Infect 2008, 14:1083–1086.PubMedCrossRef 27. Boyd EF, Hartl DL: Chromosomal regions specific to pathogenic isolates of Escherichia coli have a phylogenetically clustered distribution. J Bacteriol 1998, 180:1159–1165.PubMed 28. Le Gall T, Clermont O, Gouriou S, Picard B, Nassif X, Denamur E, Tenaillon O: Extraintestinal virulence is a coincidental CUDC-907 by-product of commensalism in B2 phylogenetic group Escherichia coli strains.

Mol Biol Evol 2007, 24:2373–2384.PubMedCrossRef 29. Bidet P, Mariani-Kurkdjian P, Grimont F, Brahimi N, Courroux C, Grimont P, Bingen E: Characterization of Escherichia coli O157: H7 isolates causing haemolytic uraemic syndrome in France. J Med Microbiol 2005, 54:71–75.PubMedCrossRef 30. Hassan WM, Ellender RD, Wang SY: Fidelity of bacterial source tracking: Escherichia coli vs Enterococcus spp and minimizing selleck chemicals assignment of isolates from nonlibrary sources. J Appl Microbiol 2007, 102:591–598.PubMedCrossRef 31. Mohapatra B, Broersma K, Nordin R, Mazumder A: Evaluation of repetitive extragenic palindromic-PCR Pregnenolone for discrimination of fecal Escherichia coli from humans, and different domestic- and wild-animals. Microbiol Immunol

2007, 51:733–740.PubMed 32. Gordon DM: Geographical structure and host specificity in buy MDV3100 bacteria and the implications for tracing the source of coliform contamination. Microbiology 2001, 147:1079–1085.PubMed 33. Sambrook J, Fritsch EF, Maniatis T: Molecular Cloning: a laboratory manual. 2nd edition. N.Y., Cold Spring Harbor Laboratory, Cold Spring Harbor Laboratory Press; 1998. 34. Bush AO, Lafferty KD, Lotz JM, Shostak AW: Parasitology meets ecology on its own terms: Margolis et al . revisited. J Parasitol 1997, 83:575–583.PubMedCrossRef 35. Pianka ER: The structure of lizard communities. Ann Rev Ecol Syst 1973, 4:53–74.CrossRef 36. Ayres M, Ayres JRM, Ayres DL, Santos AS: BioEstat 4.0: Aplicações estatísticas nas áreas das ciências biológicas e médicas. Belém: Sociedade Civil Mamirauá, CNPq; 2005. 37. StatSoft Inc: Electronic Statistics Textbook. StatSoft. [http://​www.​statsoft.​com/​textbook/​stathome.​html] 2007. 38. Rakotomalala R: TANAGRA: un logiciel gratuit pour l’enseignement et la recherché. In: Actes de EGC 2005, 2:697–702. 39.

5 fold) under iron-replete conditions in C MAP strain (Figure 3B). Discussion Johne’s disease is a major animal health problem of ruminant species worldwide and imposes significant economic losses to the industry. Our ability to culture the causative agent–Mycobacterium avium

Vactosertib subsp. paratuberculosis (MAP)–and therefore its rapid diagnosis and our understanding of its virulence is limited. MAP is difficult to culture because of its unusually strict iron requirements. For optimal growth in laboratory media, MAP requires a siderophore (mycobactin) supplementation that makes MAP fastidious [39]., often requiring eight to sixteen weeks to produce colonies in culture – a major hurdle in the diagnosis and therefore implementation of optimal control measures. Understanding iron regulatory networks in the pathogen invitro is therefore of great importance. A tale of two strain types of MAP – A case to study iron regulation Several microbiological and genotyping studies and clinical observations suggest that Johne’s in certain hosts such as sheep, goats, deer, and bison is caused by a distinct set of strains that show a relatively high degree of host preference [18, 40]. At least two microbiologically distinct types of MAP have been recognized. A less readily cultivable type is the common, but not invariable, cause of Selleckchem MDV3100 paratuberculosis in sheep (S MAP) [39, 41, 42], while

another readily cultivable type is the most common cause of the disease in ZD1839 cattle (C MAP). Cell infection

studies have also revealed distinctive host response phenotypes between cattle and sheep MAP strains – the former elicit primarily a pro-inflammatory response while latter strains suppress inflammation and upregulate anti-apoptotic pathways [24, 25]. In addition, since MAP genome sequence was published in 2005, very little research has focused on iron physiology and its contribution to metabolic networks of this fastidious organism. Based on these classical microbiologic, Cell press genotypic, and clinical observations, we addressed the hypothesis that the iron dependent gene regulation is different between cattle and sheep MAP strains using a systems approach. Iron-sparing response to iron-limitation is unique to cattle MAP strain Iron is a critical component of several metabolic enzymes [43]. Most bacteria respond to iron starvation with a unique regulatory mechanism called the iron-sparing response [35]. Iron-sparing is a physiological phenomenon used by cells to increase the intracellular iron pool by post-transcriptionally repressing the synthesis of non-essential iron using proteins and sparing iron for essential cellular functions [44]. Therefore, the paradigm is to transcriptionally upregulate all iron uptake systems while repressing non-essential enzymes via post-transcriptional regulatory mechanisms to survive iron-limiting conditions.

Also, γ 1=−3.2e V and γ 3=−0.3e V refer to the first- and third-nearest neighbor Quisinostat ic50 hopping parameters and Δ γ 1=−0.2 eV is used for the correction to γ 1 due to edge bond relaxation effect. A poisson’s ratio value of 0.165 is used

in this study [31]. The electron effective mass AG-881 supplier of each conduction subband can be calculated by using the formula (4) and at the bottom of the conduction band is given by (5) Figure 2 illustrates the dependence of band gap E G,n of the GNR’s family N=3p+1 on the uniaxial tensile strain ε. As it is seen, in the range of tensile strain 0%≤ε≤15%, E g decreases first and then increases linearly. Therefore, there is a turning point, i.e., as the strain increases, there is an abrupt reversal in the sign of dE g /d ε, making the curves to display a V shape. The turning point moves toward smaller values of strain as the width of the AGNR increases. Moreover, the slope of E g (ε) is almost identical for various N and the peak value decreases see more with increasing N. The above observations are in agrement with the main features revealed by using tight-binding or first-principles numerical calculations [17, 20]. On the other hand, Figure 3 shows the variation of effective mass at the conduction band minimum with strain ε. As it is clearly seen, has similar strain dependence as E g and a linear

relation between and E g is expected which could be correlated to an inverse relationship Amisulpride between mobility and band gap [32]. These effective mass variations is attributed to the change in the conduction band minimum position under various strain values. Figure 2 Band gap variation versus uniaxial tensile strain for different (3 p +1)-GNRs with indices p =3,4,5,6. Figure 3 Effective mass variation versus uniaxial tensile strain for different (3 p +1)-GNRs with indices p =3,4,5,6. Device performance Assuming a ballistic channel, the carriers with +k and −k states are in equilibrium with Fermi energies of the source (E FS) and the drain (E FD), respectively, with E

FS=E F and E FD=E F−qV D. The carrier density inside the channel can be obtained by employing the effective-mass approximation and integrating the density of states over all possible energies [26] (6) where F j is the Fermi-Dirac integral of order j defined as (7) and η n,S =(E FS−E C,n )/k B T, η n,D=(E FD−E C,n )/k B T. Considering the electrostatics describing the structure, the following relation between the gate voltage and Fermi energy E F can be obtained [33] (8) where q is the carrier charge, C ins is the gate-insulator capacitance per unit length of the GNR and V FB denotes the flat-band voltage. The value of V FB depends on the work function difference between the metal-gate electrode and the GNR, and it can be set simply to zero as it is discussed in detail in [34].

At each sampling point, LB agar was pre-contaminated with A. baumannii M3237 suspension to obtain surface concentrations

of 5 × 101, 5 × 102, and 5 × 103 CFU/ml. Contaminated agar plates were dried for 30 min in a biosafety hood at room temperature and divided into two groups: test agars received 0.1 or 0.5 ml of the phage-containing lotion to simulate the volumes of lotion used by most hand cream consumers and control. The control agars consisted of a phage-free lotion. The OSI-906 ic50 test and control agars were then incubated for 24 h at 37°C, and bacterial recovery counts calculated by comparing the number of A. baumannii M3237 colonies from the test agars with those from the control agars. ϕAB2 in glycerol as a hand sanitizer Briefly, the phage stock was mixed with glycerol to obtain a solution of 10% (v/v) glycerol/108 PFU/ml phage and stored at room temperature for up to 180 days to obtain a kinetic curve of the phage variation during this period. Phage stability and ability to inhibit A. baumannii M3237 was determined as described above for lotions. Statistical analysis Statistical analyses

were performed using SPSS, version click here 17.0 (SPSS Institute Inc., Chicago, IL, USA). Measurement of ϕAB2 bactericidal effect in liquid suspensions and glass slides, comparison of A. baumannii M3237 survival rates with different incubation times and control sets and reduction of viable A. baumannii M3237 by ϕAB2 lotion or glycerol was performed using one-way ANOVA, followed by Tukey’s test. Acknowledgments We thank Prof. Yi-Hsiung Tseng for critical reading of our manuscript. This work was

supported by grant NSC 100-2314-B-320-003 from the National Science Council, Republic of China; grant TCSP99-03-05 from Buddhist Tzu Chi General Hospital; and grant TCIRP98003-03 from Tzu Chi University. Yu-Lin Liu was supported by a graduate scholarship from the latter grant during part of this research project. References 1. Bergogne-Berezin see more E, Towner KJ: Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features. Clin Microbiol Rev 1996, 9:148–165.PubMed 2. Villegas MV, Hartstein AI: Acinetobacter outbreaks, 1977–2000. CP673451 order Infect Control Hosp Epidemiol 2003, 24:284–295.PubMedCrossRef 3. Okpara AU, Maswoswe JJ: Emergence of multidrug-resistant isolates of Acinetobacter baumannii . Am J Hosp Pharm 1994, 51:2671–2675.PubMed 4. Gaynes R, Edwards JR: Overview of nosocomial infections caused by gram-negative bacilli. Clin Infect Dis 2005, 41:848–854.PubMedCrossRef 5. Meric M, Kasap M, Gacar G, Budak F, Dundar D, Kolayli F, Eroglu C, Vahaboglu H: Emergence and spread of carbapenem-resistant Acinetobacter baumannii in a tertiary care hospital in Turkey. FEMS Microbiol Lett 2008, 282:214–218.PubMedCrossRef 6.

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].