Moreover, data on many important variables that may influence the risk of fracture and the uptake of treatment, such as family history and lifestyle factors, are not available. In our study, patients who switched treatment have been excluded from the analysis, and this may limit the extent to which the this website findings

can be generalised to all women starting an antiresorptive therapy with bisphosphonates. Such women may switch to a treatment that they consider more acceptable, with which they may be more compliant. In our study, the proportion of women who switched treatments within the following year was 3%, lower than switch rates reported in previous studies [35] and is unlikely to have introduced significant bias. However, the adherence of switchers to their new treatment merits a dedicated study. Finally, the definition of an acceptable prescription refill gap for determining persistence rates in the study was arbitrary, even though this definition is known to exert a crucial selleckchem influence on the observed persistence. We have attempted to control for the influence of confounders on the observed differences between the monthly and weekly regimens by using propensity scoring, but it is clearly possible that unidentified confounders for which data were not collected may play a role. It should be noted that a criterion for inclusion was that women should have consulted their GP during the reference period, which may de

facto enriched the study population in more adherent patients. However, such a bias is in principle non-differential between the two groups. The study also presents a number of strengths. These include the representativity of the study sample with respect to primary care in France. In addition, multivariate analysis was Y-27632 2HCl performed to take into account the influence of potential confounding factors on the relationship between treatment regimen and adherence. The fact that the confounding factors identified were consistent with known

determinants of adherence supports the face validity of the model. In addition, sensitivity analyses were performed to determine the influence of the definition of the permissible gap on the findings. A significant relationship between treatment regimen and adherence was found with all hypotheses, supporting the robustness of this relationship. In conclusion, this study suggests that adherence to bisphosphonates is superior using a monthly treatment regimen than using a weekly one. This difference would be expected to have major repercussions on fracture protection in osteoporotic women using such treatments. However, adherence remains suboptimal and other interventions to improve adherence need to be identified and implemented. Acknowledgements This study was funded by Laboratoire GlaxoSmithKline and Laboratoire Roche, purveyors of ibandronate, an osteoporosis treatment. FEC and AFG are employees of Laboratoire GlaxoSmithKline.

Fig. 3 Absorption (solid) and fluorescence emission (dot) spectra of Lhca1/4 (red) and Lhca2/3 (black) native dimers at 77 K (Wientjes et al. 2011a) The X-ray structure of the PSI-LHCI complex shows that each Lhca binds 13–14 Chls molecules (Ben-Shem et al. 2003), and the biochemical data indicate for both dimers a Chl a/b ratio of 3.7, meaning that they have lower affinity for Chl b than the complexes of PSII (LHCII has a Chl a/b ratio of 1.33). The dimers also bind five carotenoids each, mainly lutein and violaxanthin and substoichiometric amounts of β-carotene, while neoxanthin is not present at all, at variance with the antenna of PSII (Wientjes and Croce 2011). The properties of

the individual Lhca’s have been studied by in vitro reconstitution

of the complexes Crenigacestat nmr of tomato and A. thaliana (Schmid et al. 1997, 2002; Croce et al. 2002; Castelletti et al. 2003) because at present it is still not possible to obtain native preparations of pure Lhca monomers. The Lhca’s seem to be stable in their dimeric form, while monomerization leads to the loss of some pigments. However, the properties of the reconstituted buy Ralimetinib monomers were shown to be in agreement with the properties of the native dimers (Wientjes and Croce 2011). Although the properties of all individual monomers differ substantially from each other, it is interesting to notice that many spectral and biochemical properties of the dimer Lhca1+4 are very similar to those of Lhca2+3. For example, Chl a/b is 3.7 for both dimers whereas the Chl a/b ratios are 4.0 for Lhca1, 6.2 for Lhca3, 1.85 for Lhca2, and 2.3 for Lhca4 (Castelletti et al. 2003). Although the general structure and pigment coordination of Lhca complexes are very similar to those of the Lhcb antennae, which are

mainly associated with PSII, Lhcas differ from Lhcbs because of the presence of low-energy absorption forms. The corresponding electronic transitions are responsible for fluorescence Etomidate emission that is 50 nm red-shifted as compared to the emission of Lhcb complexes. Lam et al. (1984) observed for the first time emission of a purified fraction containing LHCI complexes that was peaking around 730 nm at 77 K, indicating that at least one of the complexes should contain red forms. The first candidate was Lhca4 (Bossmann et al. 1997; Zhang et al. 1997; Schmid et al. 1997) as suggested both by the analysis of plants lacking individual complexes and by in vitro reconstitution. Later it was shown that also Lhca3 emits above 725 nm and that Lhca1 and Lhca2 emit at 690 and 702 nm (Ganeteg et al. 2001; Croce et al. 2002; Schmid et al. 2002; Castelletti et al. 2003). This means that all Lhca’s emit at energies below those of the antenna of PSII (680 nm). Lhca5 does not contain red forms and emits at 684 nm (Storf et al. 2005).

AcM11 produces a derivative of Acta 2930-B1 Comparisons between the

chromatogram and the averaged masses of the ions from Acta 2930-B1 pure substance and from peak IV of Streptomyces AcM11 extract, prepared as described in Methods. (a) The chromatogram of Acta 2930-B1 pure substance (blue) and the Streptomyces AcM11 extract (red). Average masses of Acta 2930-B1 pure substance and the Streptomyces AcM11 extract are in ESI-MS positive (b, d) and negative (c, e) modes. Note that the dominant masses in peak IV deviate one m/z unit from the respective values of the Acta 2930-B1 pure substance. (PDF 20 KB) Additional file 4: Heterobasidion abietinum is more sensitive to the cycloheximide producer, Streptomyces AcM11, and to cycloheximide than H. annosum. Antifungal influence of AcM11 and cycloheximide was tested in a Petri dish bioassay test against H. abietinum 331 and H. annosum 005. (a, Androgen Receptor pathway Antagonists d) Influence of AcM11 on the growth of the

fungus. AcM11 Tubastatin A chemical structure was applied on agar medium and the fungus was inoculated. The front of the fungal colony was circled by pencil. (b, e) Influence of cycloheximide on fungal growth. Methanol or in methanol dissolved cycloheximide was applied by filter paper on the top of the agar medium. Note that H. abietinum growth under the influence of 4 nmol cycloheximide is comparable to H. annosum growth with 50 nmol cycloheximide. The front of the fungal colony was circled by pencil. (c, f) Influence of cycloheximide on fungal growth on fungal growth. Extension of fungal mycelium was measured after one week of growth on cycloheximide containing medium (n = 9). Cycloheximide concentration range in the bioassay is based on the observed

production level in the AcM11 suspension culture, which was 10.2 nmol x ml-1. Note the lower levels of Orotidine 5′-phosphate decarboxylase cycloheximide applications to H. abietinum than to H. annosum. (DOC 3 MB) References 1. Berg G, Smalla K: Plant species and soil type cooperatively shape the structure and function of microbial communities in the rhizosphere. FEMS Microbiol Ecol 2009, 68:1–13.PubMedCrossRef 2. De Boer W, Folman LB, Summerbell RC, Boddy L: Living in a fungal world: impact of fungi on soil bacterial niche development. FEMS Microb Rev 2005, 29:795–811.CrossRef 3. Frey-Klett P, Burlinson P, Deveau A, Barret M, Tarkka M, Sarniguet A: Bacterial-fungal interactions: hyphens between agricultural, clinical, environmental, and food microbiologists. Microbiol Mol Biol Rev 2011, 75:583–609.PubMedCrossRef 4. Kinkel LL, Bakker MG, Schlatter DC: A coevolutionary framework for managing disease-suppressive soils. Annu Rev Phytopathol 2011, 49:47–67.PubMedCrossRef 5. Frey-Klett P, Garbaye J, Tarkka M: The mycorrhiza helper bacteria revisited. New Phytol 2007, 176:22–36.PubMedCrossRef 6. Doumbou CL, Hamby-Salove MK, Crawford DL, Beaulieu C: Actinomycetes, promising tools to control plant diseases and to promote plant growth. Phytoprotection 2001, 82:85–102.CrossRef 7.

One explanation for these limitations is a buy eFT508 potential link between antiangiogenic therapy and increased metastasis [5]. In RIP-Tag2 mice treated with the VEGF receptor 2-inhibitor DC101, although tumors were smaller, they showed significantly more invasive and malignant phenotypes, with most showing wide fronts of invasion into urrounding acinar tissues [6]. Rodents treated with an anti-VEGF antibody showing a striking

increase in the number and total area of small satellite tumors compared with those that had not received antiangiogenic therapy, and tumor cells often had migrated over long distances [7, 8]. Together, these results suggest that antiangiogenic therapy may influence the progression of metastatic disease. To understand the reasons for these observations and to enable enduring benefits of antiangiogenic therapies, we examined the effect of a VEGF-neutralizing antibody on metastasis in mice after short-term administration. Furthermore, the hypoxic response and vasculogenic mimicry (VM) formation were assessed in this study. Materials Antibodies GS1101 For western blotting and

histopathological analyses, a mouse anti-HIF-1α monoclonal antibody was purchased from Novus Biologicals (Littleton, CO, USA), CD34 monoclonal antibody from Abgent (San Diego, CA, USA). Cell lines The human ovarian cancer cell line SKOV3 was purchased from the ATCC and transfected with a luciferase-expressing lentivirus containing an independent open-reading frame of GFP. After 72 hours, cells were examined by fluorescence microscopy to confirm infection. Luciferase expression was determined using luciferin and an in vivo imaging system (Xenogen). Cells were maintained in RPMI-1640 medium supplemented with 10% heatinactivated fetal bovine serum (Gibco Invitrogen Corp), and incubated at 37°C in a humidified atmosphere containing 5% CO2. Three-dimensional(3D) PAK5 cultures Matrigel (BD Biosciences) was placed

dropwise onto glass coverslips in 12-well culture plates and allowed to polymerize for 30 min at 37°C. SKOV3 cells were then seeded onto the 3D matrix in complete medium. Animal models SKOV3LUC+ cells (1.2 × 106 cells) were directly injected into the tail vein of 6- 8-week-old female nude mice. Forty mice were assigned into four groups(A, B, C and D). Group A was treated with phosphate-buffered saline (PBS) bi-weekly for 3 weeks. Group B was treated with 40 mg/kg bevacizumab bi-weekly for 3 weeks. Group C was treated with 3 mg/kg cisplatin weekly for 3 weeks. Group D was treated with both bevacizumab bi-weekly and cisplatin weekly for 3 weeks. Bevacizumab and cisplatin were administered intraperitoneally. Body weight was measured and recorded weekly. Metastatic disease progression in SKOV3LUC+ tumor-bearing mice was monitored. Before mice were anesthetized with Forane, an aqueous solution of luciferin (150 mg/kg) was intraperitoneally injected at 10 min prior to imaging.

Nobile et al.[30] found that the expression of Hwp1 in Saccharomyces cerevisiae permits adherence to wild-type C. albicans but not an als1Δ/als1Δ als3Δ/als3Δ double selleck products mutant. In addition, a TDH3-HWP1 hybrid gene could not promote biofilm formation in the als1Δ/als1Δ als3Δ/als3Δ background in vitro or in vivo. Our study revealed that human serum decreased the expression level

of ALS1 and ALS3, so overexpression of HWP1 failed to save the adhesion and biofilm formation of C. albicans. ECE1 was regarded as a hyphal-induced gene, although its mechanism of action is uncertain. Our study showed that hyphae were significantly greater in the presence of serum than in the control group, especially in the mature biofilm stage (data not shown). This may be due to the increase of ECE1 and HWP1[23]. In this study, we also tested the expression of adhesion-related genes in biofilms grown for 24 h and found that the expression trend of related genes at this time was similar to the adhesion phase, both in the reduction of ALS1 and ALS3 and the up-regulation of HWP1 and ECE1. The expression of the BCR1 gene, however, was significantly inhibited. Adriamycin solubility dmso Its level was far lower than that of the control group. All in all, the serum reduces BCR1 gene expression,

and that might be a reason for biofilm inhibition. Conclusion In summary, our study demonstrated that human serum may reduce the biofilm formation of C. albicans by inhibiting Cyclin-dependent kinase 3 adhesion. This inhibition is partly due to the down-regulation of adhesion-related genes, including ALS1, ALS3 and BCR1. Meanwhile, the inhibitory effect of human serum is caused by non-protein

components in the serum. Therefore, biofilm formation in vivo may be “selected for” (possibly by immune pressure and sheer forces) rather than “induced” by serum at the level of transcription. Methods Ethics Statement This study was approved by the Medical Ethics Committee of Beijing Friendship Hospital, Capital Medical University, Beijing, China (approval #BJFH-EC/2013-014), and individual informed consent was waived. Organisms Four Candida albicans strains (laboratory strain ATCC90028 and three clinical isolates of C. albicans: 9079, y2991, 31448) were tested in this study. The three C. albicans bloodstream isolates were collected from three different intensive care patients admitted to the Beijing Friendship Hospital and were confirmed according to standard mycological methods, such as the germ tube test in serum, growth on CHROMagar Candida medium, and API testing methods. All isolates were stored in skim milk at -80°C until use. Medium and growth conditions Prior to each experiment, C. albicans strains were subcultured on Sabouraud’s Agar (SDA) at 35°C for 24 h.

Proc Natl Acad Sci USA 2009, 106:5859–5864.PubMedCrossRef 28. de Vrije T, Mars AE, Budde MA, Lai MH, Dijkema C, de Waard P, Claassen PA: Glycolytic pathway and hydrogen yield studies of the extreme thermophile Caldicellulosiruptor saccharolyticus. Appl Microbiol Biotechnol 2007, 74:1358–1367.PubMedCrossRef 29. Howell BF, McCune S, Schaffer R: Lactate-to-pyruvate or pyruvate-to-lactate assay for lactate dehydrogenase: a re-examination. Clin Chem 1979, 25:269–272.PubMed 30.

Ma K, Hutchins A, Sung SJ, Adams MW: Pyruvate ferredoxin oxidoreductase from the hyperthermophilic JNK-IN-8 in vitro archaeon, Pyrococcus furiosus , functions as a CoA-dependent pyruvate decarboxylase. Proc Natl Acad Sci USA 1997, 94:9608–9613.PubMedCrossRef 31. Tang KH, Wen J, Li X, Blankenship

RE: Role of the AcsF protein in Chloroflexus aurantiacus . J Bacteriol 2009, 191:3580–3587.PubMedCrossRef 32. Bradford MM: A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 1976, 72:248–254.PubMedCrossRef 33. Ainsworth S, MacFarlane N: A kinetic study of rabbit muscle pyruvate kinase. Biochem J 1973, 131:223–236.PubMed 34. Cassan N, Lagoutte B, Setif P: Ferredoxin-NADP+ reductase. Kinetics of electron transfer, SPTLC1 transient intermediates, and catalytic activities BIX 1294 studied by flash-absorption spectroscopy with isolated photosystem I and ferredoxin. J Biol Chem 2005, 280:25960–25972.PubMedCrossRef 35. Chen ZH, Walker RP, Tecsi LI, Lea PJ, Leegood RC: Phosphoenolpyruvate carboxykinase in cucumber plants is increased both by ammonium and by acidification, and is present in the phloem. Planta 2004, 219:48–58.PubMedCrossRef 36. Van Schaftingen E, Jett MF, Hue L, Hers HG: Control

of liver 6-phosphofructokinase by fructose 2,6-bisphosphate and other effectors. Proc Natl Acad Sci USA 1981, 78:3483–3486.PubMedCrossRef 37. Gerber G, Preissler H, Heinrich R, Rapoport SM: Hexokinase of human erythrocytes. Purification, kinetic model and its application to the conditions in the cell. Eur J Biochem 1974, 45:39–52.PubMedCrossRef 38. Kumari S, Tishel R, Eisenbach M, Wolfe AJ: Cloning, characterization, and functional expression of acs, the gene which encodes acetyl coenzyme A synthetase in Escherichia coli. J Bacteriol 1995, 177:2878–2886.PubMed 39. Kuang Y, Salem N, Wang F, Schomisch SJ, Chandramouli V, Lee Z: A colorimetric assay method to measure acetyl-CoA synthetase activity: application to woodchuck model of hepatitis virus-induced hepatocellular carcinoma. J Biochem Biophys Methods 2007, 70:649–655.

Besides its large size and the associated high mortality click here rate, these two outbreaks are unique in that a large proportion of patients were victim to streptococcal toxic shock syndrome (STSS) [7]. Before that, STSS has been limited to disease caused by the group A streptococcus [9], S. suis (nongroup A) has not previously been linked to STSS. To get insight into the high virulence of the S. suis isolates emerged in China, we previously decoded the whole genomic sequence of two epidemic strains (98HAH12 and 05ZYH33) isolated from the 1998 and 2005 Chinese outbreaks respectively, and identified a pathogenicity island (PAI) designated 89K that is specific for Chinese outbreak isolates [10, 11]. Subsequently,

we provided genetic evidence showing that an 89K-borne type IV secretion system (T4SS) forms an important pathway for horizontal transfer of 89K and secretion of some unknown pathogenic effectors that are responsible for STSS caused by the highly virulent S. suis 2 strains [12, 13]. However, the 89K T4SS assembly process in vivo and in vitro remains largely unknown. There has long been a general lack of knowledge of T4SS functions and cellular localization in gram-positive bacteria [14]. It has been suggested that the assembly processes

must be similar to or even simpler than those in gram-negative bacteria [15, 16]. In the well-characterized model for the Agrobacterium tumefaciens VirB/D T4SS, the VirB1 component functions as a lytic transglycosylase

that can digest the peptidoglycan layer of cell wall, thus facilitating the assembly of envelope-spanning protein complex of T4SS under temporal and spatial control [17, 18]. Among Captisol the single operon composed of 15 genes that encodes the functional T4SS in S. suis 89K PAI, only the virB1-89K gene product shows similarity to the Agrobacterium VirB1 component and contains a conserved cysteine, histidine-dependent amidohydrolases/peptidases (CHAP) domain that may function in peptidoglycan hydrolysis [19]. We once proposed that VirB1-89K should function to punch holes in the peptidoglycan Sodium butyrate cell wall to allow the assembly of the T4SS apparatus [12]. However, we did not provide direct evidence to support this hypothesis. In the present study, therefore, we expressed and purified the CHAP domain of VirB1-89K in Escherichia coli, and tested its putative peptidoglycan hydrolysis activity in vitro. Furthermore, an isogenic knockout mutant of virB1-89K and its complementary strain were used in a mouse infection model to assess the contribution of VirB1-89K to the virulence of S. suis outbreak strain. The experimental results indicated that VirB1-89K facilitates the assembly of 89K T4SS apparatus by catalyzing the degradation of the peptidoglycan cell wall, thus contributing to the pathogenesis of T4SS in the S. suis. Results Characterization of the CHAP domain of VirB1-89K On the negative strand of the 89K PAI in the genome of S.

(iii)

E. coli strain S17-1 transformed with pSUPpX2 was conjugated with MSR-1 as described previously SBI-0206965 [18]. The final Gmr CmS colonies, confirmed by PCR, comprised a double-crossover recombination mamX deletion mutant (∆mamX). To complement the mutant, the mamX gene (primers: X-F, 5′AACTGCAGTTGACCACAGTCGAACTCCC3′; X-R, 5′CGCGGATCCTATTCCATTG GGTGGGAGCG3′) was cloned into pRK415 by PstI and BamHI sites, and the resulting plasmid pRK415X was transferred into E. coli S17-1 (restriction sites are underlined). The subsequent conjugation was performed as described above. The Gmr Tcr colonies, confirmed by PCR, were complemented strains (termed CmamX). Transmission electron microscopy Cells were placed on a copper grid, washed twice with distilled water, dried, and observed by TEM (Philips Tecnai F30, Eindhoven, Netherlands). For HR-TEM (JEOL 2010, Tachikawa, Tokyo), a carbon grid was used. Measurement of iron content Each strain was cultured microaerobically at 30°C in OFM. After the cultures reached stationary phase, 10-ml samples were centrifuged at 10,000 x g for 2 min. The pellets were washed three times with distilled water, dried to a constant weight and nitrified in 1 ml

nitric acid for 3 hr as described previously [40]. Intracellular iron content was assayed using an Inductively Coupled Plasma Optical Emission Spectrometer (ICP-OES; Optima 5300DV; Perkin Elmer, Waltham, MA, USA). The iron percentage of cells was calculated as iron content divided by dry weight. Rock magnetic measurements Cell cultures were centrifuged (10,000 x g) https://www.selleckchem.com/products/ferrostatin-1-fer-1.html at 4°C for 5 min, and the pellets were subjected to magnetic measurements. Room-temperature

hysteresis loops and first-order reversal curves (FORCs) were measured by an Alternating Gradient Force Magnetometer Model buy Rucaparib MicroMag 2900 (Princeton Measurements Corp., Princeton, NJ, USA; sensitivity 1.0×10−11 Am2) as described previously [22]. Quantitative real-time RT-PCR (qPCR) Total RNA was purified using TRIzol Reagent (Invitrogen Corp., Carlsbad, CA, USA) according to the manufacturer’s instructions. The remaining genomic DNA in RNA preparations was degraded by DNase I (Takara, Shiga, Japan). cDNA synthesis was performed using M-MLV reverse transcriptase, dNTPs, and random primers (Promega Corp., San Luis Obispo, CA, USA) according to the manufacturer’s instructions. A LightCycler 480 Instrument II (Roche, South San Francisco, CA, USA) was used for qPCR. The LightCycler 480 SYBR Green I Master kit (Roche) was used as the manual. In a 20-μl PCR system, the template cDNA content was set below 500 ng and that of each oligo as 0.5 μM. The reaction program consisted of initial denaturation at 95°C for 10 min, followed by 40 cycles of denaturation at 95°C for 15 sec, annealing at 62°C for 5 sec, extension at 72°C for 15 sec, and fluorescence measurement at 76°C for 3 sec.

Aust J Plant Physiol 24:17–25CrossRef Yin

ZH, Johnson GN (2000) Photosynthetic acclimation of higher plants to growth in fluctuating light environments. Photosynth Res 63:97–107PubMedCrossRef Yoshida K, Watanabe CK, Hachiya T, Tholen D, Shibata M, Terashima I, Noguchi K (2011) Distinct responses of the mitochondrial respiratory chain to long- PI3K Inhibitor Library and short-term high light environments in Arabidopsis thaliana. Plant Cell Environ 34:618–628PubMedCrossRef”
“A beloved wife, mother and grandmother, and a very dear friend and colleague, has unexpectedly left us, much too early (see Fig. 1). Margareta Ryberg, née Kvist, was born on April 14, 1946 in Göteborg, Sweden. After graduating from high school Daporinad ic50 in 1966, Margareta continued her studies with zoology, botany, and chemistry at the University of Göteborg. During one of the first courses,

Margareta met her husband to-be, Hans (co-author of this Tribute), and they married in 1969. Margareta and Hans continued studying botany in Göteborg and were both hired as teaching assistants before their postgraduate studies. Margareta defended her PhD thesis in Plant Physiology in 1982. Her thesis was under the supervision of Hemming Virgin and Christer Sundqvist. After her doctoral degree, she continued to work in the same department throughout her professional career. Margareta spent a few research periods abroad. In Kiel, Germany, she worked with Klaus Apel (now at the Boyce Thompson Institute in Ithaca, NY, USA) and with Flucloronide Katayoon (Katie) Dehesh (now at University of California at Davis, CA, USA; see Dehesh and Ryberg 1985; Ryberg and Dehesh 1986; Dehesh et al. 1986). Katie came to be like a sister to Margareta. Fig. 1 Margareta Ryberg by the Tiber, Rome, January 2010. Photo by Britta Skagerfält,

co-author of this Tribute, and daughter of Margareta Over the years, Margareta was given an ever-greater responsibility for the teaching of plant physiology at the University of Göteborg. Devoted and demanding, she remained highly appreciated by her students. In research, Margareta consistently followed a theme which had also occupied one of us (LOB) in the early days: the different forms of protochlorophyll(ide), their protein partners, and their transformations in angiosperms. Etioplasts from wheat were fractionated by differential and density gradient centrifugations, and the fractions analyzed by many different methods, in particular absorption, fluorescence, and circular dichroism spectrophotometry (Böddi et al. 1989, 1992). Eventually her studies became concerned with structural aspects and the nature of prolamellar bodies.

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the LPS/IFNgamma-induced release of NO and TNFalpha. FEBS Lett 1999, 462:199–204.PubMedCrossRef 46. Grassl GA, et al.: Activation of NF-kappaB and IL-8 by Yersinia enterocolitica invasin protein is conferred by engagement of Rac1 and MAP kinase cascades. Cell Microbiol 2003, 5:957–971.PubMedCrossRef 47. Schulte R, et al.: Yersinia enterocolitica invasin protein triggers IL-8 production in epithelial cells via activation of Rel p65-p65 homodimers. FASEB J 2000, 14:1471–1484.PubMedCrossRef 48. Monnazzi LG, Carlos IZ, de Medeiros BM: Influence of Yersinia pseudotuberculosis outer proteins (Yops) on interleukin-12, tumor necrosis factor alpha and nitric oxide production by peritoneal macrophages. Immunol Lett 2004, 94:91–98.PubMedCrossRef 49. Auerbuch V, Golenbock DT, Isberg RR: Innate immune recognition of Yersinia pseudotuberculosis type III secretion. PLoS Pathog 2009, 5:e1000686.PubMedCrossRef 50. Bergsbaken T, Cookson BT: Macrophage activation redirects yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis. PLoS Pathog 2007, 3:e161.PubMedCrossRef 51.