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Several Pathogens (several + pathogen)
Selected AbstractsIron enhances endothelial cell activation in response to Cytomegalovirus or Chlamydia pneumoniae infectionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006A. E. R. Kartikasari Abstract Background, Chronic inflammation has been implemented in the pathogenesis of inflammatory diseases like atherosclerosis. Several pathogens like Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) result in inflammation and thereby are potentially artherogenic. Those infections could trigger endothelial activation, the starting point of the atherogenic inflammatory cascade. Considering the role of iron in a wide range of infection processes, the presence of iron may complicate infection-mediated endothelial activation. Materials and methods, Endothelial intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) expression were measured using flow cytometry, as an indication of endothelial activation. Cytotoxicity was monitored using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Immunostaining was applied to measure Cp and CMV infectivity to endothelial cells. Results, An increased number of infected endothelial cells in a monolayer population leads to a raised expression of adhesion molecules of the whole cell population, suggesting paracrine interactions. Iron additively up-regulated Cp-induced VCAM-1 expression, whereas synergistically potentiated Cp-induced ICAM-1 expression. Together with CMV, iron also enhanced ICAM-1 and VCAM-1 expression. These iron effects were observed without modulation of the initial infectivity of both microorganisms. Moreover, the effects of iron could be reversed by intracellular iron chelation or radical scavenging, conforming modulating effects of iron on endothelial activation after infections. Conclusions, Endothelial response towards chronic infections depends on intracellular iron levels. Iron status in populations positive for Cp or CMV infections should be considered as a potential determinant for the development of atherosclerosis. [source] Mycobacterium tuberculosis possesses a functional enzyme for the synthesis of vitamin C, L -gulono-1,4-lactone dehydrogenaseFEBS JOURNAL, Issue 19 2006Beata A. Wolucka The last step of the biosynthesis of l -ascorbic acid (vitamin C) in plants and animals is catalyzed by l -gulono-1,4-lactone oxidoreductases, which use both l -gulono-1,4-lactone and l -galactono-1,4-lactone as substrates. l -Gulono-1,4-lactone oxidase is missing in scurvy-prone, vitamin C-deficient animals, such as humans and guinea pigs, which are also highly susceptible to tuberculosis. A blast search using the rat l -gulono-1,4-lactone oxidase sequence revealed the presence of closely related orthologs in a limited number of bacterial species, including several pathogens of human lungs, such as Mycobacterium tuberculosis, Pseudomonas aeruginosa, Burkholderia cepacia and Bacillus anthracis. The genome of M. tuberculosis, the etiologic agent of tuberculosis, encodes a protein (Rv1771) that shows 32% identity with the rat l -gulono-1,4-lactone oxidase protein. The Rv1771 gene was cloned and expressed in Escherichia coli, and the corresponding protein was affinity-purified and characterized. The FAD-binding motif-containing Rv1771 protein is a metalloenzyme that oxidizes l -gulono-1,4-lactone (Km 5.5 mm) but not l -galactono-1,4-lactone. The enzyme has a dehydrogenase activity and can use both cytochrome c (Km 4.7 µm) and phenazine methosulfate as exogenous electron acceptors. Molecular oxygen does not serve as a substrate for the Rv1771 protein. Dehydrogenase activity was measured in cellular extracts of a Mycobacterium bovis BCG strain. In conclusion, M. tuberculosis produces a novel, highly specific l -gulono-1,4-lactone dehydrogenase (Rv1771) and has the capacity to synthesize vitamin C. [source] The Potential Use of a Silicon Source as a Component of an Ecological Management of Coffee PlantsJOURNAL OF PHYTOPATHOLOGY, Issue 7-8 2008J. C. Martinati Abstract Coffee is one of the most important agricultural export commodities in the world and it represents the main export from some developing countries. Therefore, the development of new methods of coffee management that improves production without causing any damage to the environment is an attractive alternative for producers. Much effort has been invested towards understanding the mode of action of compounds that can induce resistance against several pathogens without injuring the environment. Many researches have considered silicon efficient in avoiding plant pathogen penetration and development. Our aim was to verify the effect of potassium silicate and calcium/magnesium silicate in the development of coffee seedlings (Coffea arabica cv. Mundo Novo) as well as to evaluate the incidence of coffee leaf rust development under greenhouse conditions. The experiment was a completely randomized design with 12 treatments with 10 plants per treatment. The treatments were 0, 0.25, 1.25, 2.5, 4 and 5 ,m of Si for each source of silicon incorporated into the soil. The seedlings were inoculated with a urediniospores suspension of Hemileia vastatrix (2 mg/ml) at the seventh month after planting (six pair of leaves). Evaluations were performed by counting the number of lesions per leaf. The statistical analysis showed that the number of lesions reduced by up to 66% at the highest silicon dose when compared to the number of lesions in control plants. Infected plants were found to have a linear decrease of lesions with the increase of silicate concentration. The lowest number of lesions per leaf area was observed in plants that received 5 ,m of Si from potassium silicate. This result indicates the use of silicon as an alternative for an ecological management system for coffee disease protection. [source] Incidence of Cotton Seedling Diseases Caused by Rhizoctonia solani and Thielaviopsis basicola in Relation to Previous Crop, Residue Management and Nutrients Availability in Soils in SW SpainJOURNAL OF PHYTOPATHOLOGY, Issue 11-12 2005A. Delgado Abstract Cotton seedling damping-off is considered a disease complex, in which several pathogens can be involved. In SW Spain, postemergence damping-off seems to be mainly associated with Rhizoctonia solani and Thielaviopsis basicola, posing a serious limitation for crop, especially in cold springs. Ninety-seven commercial plots, where postemergence damping-off of cotton seedlings was observed during previous years, were selected in April 2001. In each plot, plants were randomly sampled between cotyledon to three true-leaf stage and soil samples besides the plants were taken. Symptomatic plants were separated according to the main observable seedling disease symptom: black necrosis (black root rot), brown necrosis and other symptoms. Thielaviopsis basicola inoculum was estimated in soil samples. Soil samples were also analysed for nutrient availability (N, P, K, Ca, Mg, Fe, Cu, Mn and Zn). All the sampled plants showed some seedling disease symptom. Macroscopic symptoms can provide a reasonable distinction between these two major pathogens involved in seedling disease symptoms in the studied area: the percentage of T. basicola isolates (18%) from black necrosis symptomatic plants was significantly higher than that of R. solani (4.1%), whereas in brown necrosis symptomatic plants, the situation was reversed (10.7 vs. 12.8%). The percentage of plants with black necrosis symptoms was inversely related to the portion of plants with brown necrosis in each plot. The mean incidence of black necrosis was significantly lower in plots with residue incorporation (sugar beet as the preceding crop) than in plots without residue incorporation. No significant effect of preceding crop or residue management on brown necrosis incidence was observed. Incidence of black necrosis was negatively correlated with available N measured as NO3 -N when corn or sunflower were the preceding crop. The incidence of black necrosis was positively related to Fe availability in soil after cotton as preceding crop, whereas brown necrosis was negatively related to the availability of this micronutrient. [source] Proinflammatory signalling stimulated by the type III translocation factor YopB is counteracted by multiple effectors in epithelial cells infected with Yersinia pseudotuberculosisMOLECULAR MICROBIOLOGY, Issue 5 2003Gloria I. Viboud Summary Type III secretion systems are used by several pathogens to translocate effector proteins into host cells. Yersinia pseudotuberculosis delivers several Yop effectors (e.g. YopH, YopE and YopJ) to counteract signalling responses during infection. YopB, YopD and LcrV are components of the translocation machinery. Here, we demonstrate that a type III translocation protein stimulates proinflammatory signalling in host cells, and that multiple effector Yops counteract this response. To examine proinflammatory signalling by the type III translocation machinery, HeLa cells infected with wild-type or Yop,Y. pseudotuberculosis strains were assayed for interleukin (IL)-8 production. HeLa cells infected with a YopEHJ, triple mutant released significantly more IL-8 than HeLa cells infected with isogenic wild-type, YopE,, YopH, or YopJ, bacteria. Complementation analysis demonstrated that YopE, YopH or YopJ are sufficient to counteract IL-8 production. IL-8 production required YopB, but did not require YopD, pore formation or invasin-mediated adhesion. In addition, YopB was required for activation of nuclear factor kappa B, the mitogen-activated protein kinases ERK and JNK and the small GTPase Ras in HeLa cells infected with the YopEHJ, mutant. We conclude that interaction of the Yersinia type III translocator factor YopB with the host cell triggers a proinflammatory signalling response that is counteracted by multiple effectors in host cells. [source] Wolbachia surface protein (WSP) inhibits apoptosis in human neutrophilsPARASITE IMMUNOLOGY, Issue 2 2007C. BAZZOCCHI SUMMARY Polymorphonuclear cells (PMNs) are essential for the innate immune response against invading bacteria. At the same time, modulation of PMNs' apoptosis or cell death by bacteria has emerged as a mechanism of pathogenesis. Wolbachia bacteria are Gram-negative endosymbionts of filarial nematodes and arthropods, phylogenetically related to the genera Anaplasma, Ehrlichia and Neorickettsia (family Anaplasmataceae). Although several pathogens are known to interfere with apoptosis, there is only limited information on specific proteins that modulate this phenomenon. This is the first evidence for the anti-apoptotic activity of a surface protein of Wolbachia from filarial nematode parasites (the Wolbachia surface protein, WSP). The inhibition of apoptosis was demonstrated on purified human PMNs in vitro by different methods. TUNEL assay showed that the percentage of dead cells was reduced after stimulation with WSP; Annexin V-FITC binding assay confirmed that cell death was due mainly to apoptosis and not to necrosis. Reduced caspase-3 activity in stimulated cells also confirmed an inhibition of the apoptotic process. [source] QTL for resistance to summer mortality and OsHV-1 load in the Pacific oyster (Crassostrea gigas)ANIMAL GENETICS, Issue 4 2010C. Sauvage Summary Summer mortality is a phenomenon severely affecting the aquaculture production of the Pacific oyster (Crassostrea gigas). Although its causal factors are complex, resistance to mortality has been described as a highly heritable trait, and several pathogens including the virus Ostreid Herpes virus type 1 (OsHV-1) have been associated with this phenomenon. A QTL analysis for survival of summer mortality and OsHV-1 load, estimated using real-time PCR, was performed using five F2 full-sib families resulting from a divergent selection experiment for resistance to summer mortality. A consensus linkage map was built using 29 SNPs and 51 microsatellite markers. Five significant QTL were identified and assigned to linkage groups V, VI, VII and IX. Analysis of single full-sib families revealed differential QTL segregation between families. QTL for the two-recorded traits presented very similar locations, highlighting the interest of further study of their respective genetic controls. These QTL show substantial genetic variation in resistance to summer mortality, and present new opportunities for selection for resistance to OsHV-1. [source] Expression, crystallization and preliminary crystallographic analysis of SufE (XAC2355) from Xanthomonas axonopodis pv. citriACTA CRYSTALLOGRAPHICA SECTION F (ELECTRONIC), Issue 3 2006Cristiane R. Guzzo Xanthomonas axonopodis pv. citri (Xac) SufE (XAC2355) is a member of a family of bacterial proteins that are conserved in several pathogens and phytopathogens. The Escherichia coli suf operon is involved in iron,sulfur cluster biosynthesis under iron-limitation and stress conditions. It has recently been demonstrated that SufE and SufS form a novel two-component cysteine desulfarase in which SufS catalyses the conversion of l -cysteine to l -alanine, forming a protein-bound persulfide intermediate. The S atom is then transferred to SufE, from which it is subsequently transferred to target molecules or reduced to sulfide in solution. Here, the cloning, expression, crystallization and phase determination of Xac SufE crystals are described. Recombinant SufE was crystallized in space group P212121 and diffracted to 1.9,Å resolution at a synchrotron source. The unit-cell parameters are a = 45.837, b = 58.507, c = 98.951,Å, , = , = , = 90°. The calculated Matthews coefficient indicated the presence of two molecules in the asymmetric unit. Phasing was performed by molecular-replacement using E. coli SufE as a model (PDB code 1mzg) and an interpretable map was obtained. [source] Mimicking small G-proteins: an emerging theme from the bacterial virulence arsenalCELLULAR MICROBIOLOGY, Issue 3 2008Neal M. Alto Summary The identification of the Ras superfamily of small molecular weight GTPases (G-proteins) has opened up new fields in cancer biology, immunity and infectious disease research. Because of their ubiquitous role in cellular homeostasis, small G-proteins are common targets for several pathogens, including bacteria. It is well known that pathogenic bacteria have evolved virulence factors that chemically modify GTPases or directly mimic the activities of key regulatory proteins. However, recent studies now suggest that bacterial ,effector' proteins can also mimic the activities of Ras small G-proteins despite their lack of guanine nucleotide binding or GTPase enzymatic activity. The study of these unique pathogenic strategies continues to reveal novel mechanistic insights into host cellular communication networks and the role of small G-protein signalling during human infectious disease. [source] | ||||||||||||||||