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Abstract

Amoebiasis is the third worldwide disease due to a parasite. The causative agent of this disease, the unicellular eukaryote Entamoeba histolytica, causes dysentery and liver abscesses associated with inflammation and human cell death. During liver invasion, before entering the parenchyma, E. histolytica trophozoites are in contact with liver sinusoidal endothelial cells (LSEC). We present data characterizing human LSEC responses to interaction with E. histolytica and identifying amoebic factors involved in the process of cell death in this cell culture model potentially relevant for early steps of hepatic amoebiasis. E. histolytica interferes with host cell adhesion signalling and leads to diminished adhesion and target cell death. Contact with parasites induces disruption of actin stress fibers and focal adhesion complexes. We conclude that interference with LSEC signalling may result from amoeba-triggered changes in the mechanical forces in the vicinity of cells in contact with parasites, sensed and transmitted by focal adhesion complexes. The study highlights for the first time the potential role in the onset of hepatic amoebiasis of the loss of liver endothelium integrity by disturbance of focal adhesion function and adhesion signalling. Among the amoebic factors required for changed LSEC adherence properties we identified the Gal/GalNAC lectin, cysteine proteases and KERP1.

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SA , van Pelt W , Wagenaar JA , Owen RJ . Host-pathogen interactions in Campylobacter infections: the host perspective . Clin Microbiol Rev . 2008 ; 21 ( 3 ): 505 – 18 . 10.1128/CMR.00055-07 10. Havelaar AH , van Pelt W , Ang CW

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El-Zahaby, H. M., Gullner, G. and Király, Z. (1995): Effects of powdery mildew infection of barley on the ascorbate-glutathione cycle and other antioxidants in different host-pathogen interactions. Phytopathol. 85 , 1225

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Intestinal carriage of multi-drug resistant (MDR) Gram-negative bacteria including Pseudomonas aeruginosa (Psae) constitutes a pivotal prerequisite for subsequent fatal endogenous infections in patients at risk. We here addressed whether fecal microbiota transplantation (FMT) could effectively combat MDR-Psae carriage. Therefore, secondary abiotic mice were challenged with MDR-Psae by gavage. One week later, mice were subjected to peroral FMT from either murine or human donors on 3 consecutive days. Irrespective of murine or human origin of fecal transplant, intestinal MDR-Psae loads decreased as early as 24 h after the initial FMT. Remarkably, the murine FMT could lower intestinal MDR-Psae burdens by approximately 4 log orders of magnitude within 1 week. In another intervention study, mice harboring a human gut microbiota were perorally challenged with MDR-Psae and subjected to murine FMT on 3 consecutive days, 1 week later. Strikingly, within 5 days, murine FMT resulted in lower loads and carrier rates of MDR-Psae in mice with a human gut microbiota. In conclusion, FMT might be a promising antibiotics-independent option to combat intestinal MDR-Psae carriage and thus prevent from future endogenous infections of patients at risk.

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Abstract

Non-antibiotic feed additives including competitive exclusion products have been shown effective in reducing pathogen loads including multi-drug resistant strains from the vertebrate gut. In the present study we surveyed the intestinal bacterial colonization properties, potential macroscopic and microscopic inflammatory sequelae and immune responses upon peroral application of the commercial competitive exclusion product Aviguard® to wildtype mice in which the gut microbiota had been depleted by antibiotic pre-treatment. Until four weeks following Aviguard® challenge, bacterial strains abundant in the probiotic suspension stably established within the murine intestines. Aviguard® application did neither induce any clinical signs nor gross macroscopic intestinal inflammatory sequelae, which also held true when assessing apoptotic and proliferative cell responses in colonic epithelia until day 28 post-challenge. Whereas numbers of colonic innate immune cell subsets such as macrophages and monocytes remained unaffected, peroral Aviguard® application to microbiota depleted mice was accompanied by decreases in colonic mucosal counts of adaptive immune cells such as T and B lymphocytes. In conclusion, peroral Aviguard® application results i.) in effective intestinal colonization within microbiota depleted mice, ii.) neither in macroscopic nor in microscopic inflammatory sequelae and iii.) in lower colonic mucosal T and B cell responses.

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A F. oxysporum f. sp. dianthi strain, transformed with genes coding for fluorescent proteins (GFP or DsRedFP) as markers, was used to study the first host/pathogen interaction on carnation roots. The transformants’ mycelium observed under fluorescent light displayed a high expression of GFP and DsRedFP as a bright green or red cytoplasmic fluorescence. The root apparatus of a partially resistant cultivar of carnation was artificially inoculated by stable transformants and local colonization of plant tissues was monitored by means of fluorescence microscopy. A GFP transformed strain of F. oxysporum f. sp. dianthi allowed to follow first colonization steps on and within host root tissues. Implication of this research in studying resistance processes in carnation is discussed.

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Septoria tritici blotch (STB) caused by the fungus Mycosphaerella graminicola, is one of the most important foliar diseases of wheat (T. aestivum spp., aestivum L.). Various practices such as crop rotation, application of fungicides, and deployment of genetic resistance have been utilised to control this disease and subsequently reduce yield losses. During the last 20 years, significant progress has been made in understanding host-pathogen interaction, inheritance of STB resistance, localisation of loci controlling STB resistance and identification of molecular markers associated with STB resistance in common wheat. We review the progress made on various aspects of molecular breeding for STB resistance especially on mapping and validation of qualitative and quantitative trait loci in common wheat.

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Francisella tularensis is a Gram-negative bacterium, the causative agent of the zoonotic disease tularaemia. The bacterium has developed several extracellular and intracellular strategies to evade the hosts’ innate and adaptive immune responses. The aims of the study were to examine complement sensitivity of wild and attenuated F. tularensis ssp. holarctica strains in animal hosts of distinct sensitivity to the bacterium, to compare the complement-evading ability of wild strains of different phylogeographic background, and to examine the role of factor H in the host–pathogen interactions. Complement sensitivity assays were carried out on various F. tularensis ssp. holarctica wild strains and on the attenuated live vaccine strain (LVS) with sera of the highly sensitive house mouse (Mus musculus), the moderately sensitive European brown hare (Lepus europaeus) and the relatively resistant cattle (Bos taurus). Specific binding of complement regulator factor H to bacterial membrane proteins was examined by Western blot assays. All wild strains interacted with the hosts’ complement system and showed no significant differences in their survivability. The attenuated LVS was resistant to serum killing in mouse, but was lysed in the sera of hare and cattle. Direct binding of factor H to F. tularensis membrane proteins was not detected.

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The oil quality and yield of groundnut ( Arachis hypogaea L.) is mainly lessened by Puccinia arachidis Speg. For screening large number of genotypes to rust resistance under in vitro conditions, the present study was motivated to test and verify the reliability of certain pathogen related enzymes, alterations in protein expression level and isoenzymes, activated ahead of host pathogen interaction. Biparental segregants acquired through NCD 1 mating fashion from crosses, viz. TMV1×ICG1697 and VRI2×ICG1697 were artificially inoculated with rust pathogen. After rust infection in groundnut, the alterations in the activity of peroxidase (PO), polyphenol oxidase (PPO), ascorbic acid oxidase (AAO) and chitinase were studied at 80 and 90 days after sowing (DAS) both in susceptible and resistant segregants along with parents. Both susceptible and resistant segregants manifest increased activity of all of these three enzymes, the magnitude was higher in resistant segregants. The activity of ascorbic acid oxidase and chitinase were high at 90 DAS, while polyphenol oxidase and peroxidase exhibited maximum activity at 80 DAS. Four additional isoforms of PO and PPO and prominent expression of a 56 kDa protein were observed in resistant genotypes. The potential amount and activity of these enzymes were genetically determined and such changes in the quantity, isoenzyme and protein can be relied for screening rust tolerant genotypes in groundnut.

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Cereal Research Communications
Authors: P. Motallebi, S. Tonti, V. Niknam, H. Ebrahimzadeh, A. Pisi, P. Nipoti, M. Hashemi and A. Prodi

Fusarium culmorum is a soilborne fungal pathogen, agent of crown and root rot disease (FCRR), responsible of major economic losses in wheat plants. This host—pathogen interaction, following methyl jasmonate (MeJA) application at the beginning of the necrotrophic stage of infection, has not been previously studied at molecular level. In this study, using real-time quantitative PCR, the emerging role of MeJA in the basal resistance of two bread wheat cultivars against F. culmorum has been investigated. MeJA treatment was dispensed 6 hours after pathogen inoculation (6 hai) to detect the defense response at the beginning of the necrotrophic stage. The expression of phenylalanine ammonia-lyase (PAL), lipoxygenase (LOX), cytochrome P450 (CYP709C1) genes and of some pathogenesis related (PR) genes, including PR3, PR4 and PR9, was examined in both root and crown tissues of the susceptible wheat cultivar Falat and the tolerant cultivar Sumai3. The pathogen responsive defense genes were induced in both cultivars, with a higher level of induction in Sumai3 than in Falat. MeJA treatment reduced the symptoms in cv Falat, whereas no significant effects have been detected in cv Sumai3. In fact, MeJA treatment caused a striking difference in defense gene induction. The genetic change was present in root and crown tissues of both wheat cultivars, demonstrating a systemic signaling pathway. The chemically induced protection correlated with induction of the F. culmorum-responsive genes supports a possible role of jasmonate signaling in regulating basal resistance in wheat–F. culmorum interaction.

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