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Ubiquitous parasite of humans and endothermic animals Toxoplasma gondii (type Apicomplexa), identified by Nicolle and Manceaux over 100 years ago, is still an object of numerous extensive studies bringing very interesting and often even surprising observations as that announced in the title [1].
Toxoplasma gondii, the etiological agent of toxoplasmosis, is an Apicomplexa obligate intracellular protozoan parasite, which is able to infect any nucleated cell of numerous endothermic vertebrates. The combined abilities to actively penetrate host cells and perfectly control the fate of the parasite-containing vacuole (parasitophorus vacuole, PV) contribute to the remarkable global success of Toxoplasma as an intracellular parasite. Very broad host range and the relative ease of growth both in cell cultures in vitro and in vivo suggest that the parasite is able to manipulate the host cell apoptotic machinery. The article describes different aspects of host-parasite interplay focusing on molecular modifications of infected host cells.
Bacteriophages are an attractive tool for application in the therapy of bacterial infections, for biological control of bacterial contamination of foodstuffs in the alimentary industry, in plant protection, for control of water-borne pathogens, and control of environmental microflora. This review is mainly focused on structures governing phage recognition of host cell and mechanisms of phage adsorption and penetration into microbial cell.
During a recent survey on the protozoan blood parasites of some Egyptian reptiles, 61.04% of Acanthodactylus boskianus collected from Damietta Governorate had a hitherto undescribed species of haemogregarine which is described below as Haemogregarina damiettae sp. n. The parasitaemia was exceptionally high, allowing for detailed morphological study of various blood forms of the parasite. These stages are compared with the corresponding forms described before from Bose’s lizard.
Considering the role of lectin-carbohydrate interactions between Helicobacter pylori bacteria and the host cells we addressed the question on how mannose binding lectin - MBL, present in human plasma, may influence the phagocytosis of H. pylori by peripheral blood granulocytes. For phagocytosis assay the granulocytes separated from peripheral blood of healthy H. pylori-seronegative donors were used. Phagocytosis was estimated by fluorescence assay using FITC-labelled H. pylori cells. The MBL level in the serum samples as well as MBL-binding to H. pylori bacteria were estimated by ELISA. In this study all H. pylori isolates bound recombinant mannose binding lectin-MBL as shown by ELISA. The ingestion of H. pylori bacteria in the medium with human serum depleted in natural MBL (nMBL) was more intensive than in the medium with complete serum containing nMBL. Moreover, the ingestion of H. pylori bacteria in the medium with complete serum was increased by an addition of anti-rMBL IgG. The results indicate that interaction of bacterial and host lectins may regulate the phagocytosis of H. pylori bacteria and in this way influence an outcome of the infection caused by these microbes.
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Toxoplasma gondii and the host cells

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The protozoan Toxoplasma gondii, described by Nicolle and Manceaux in 1908, is a ubiquitous and cosmopolitan parasite that infects a wide range of mammal and bird species with high prevalence. The biological success of T. gondii is associated with the formation of a specific relationship between the parasite and host cells leading to the establishment of a latent, chronic infection. During primary infection, acquired mostly by the oral route, the quickly multiplying tachyzoites disseminate through the body crossing several structural-functional barriers as bloodbrain or blood-retina, then they transform into dormant bradyzoites which, enclosed in tissue cysts, occupy preferentially the brain, skeletal muscle and eye. Although T. gondii is able to infect all kinds of nucleated cells, it uses strictly defined host cells, dependent on the life-cycle phase and infection stage. The article discusses selected aspects of the parasite passing via the host body barriers as well as particular role of dendritic cells and skeletal muscle cells, used by the parasite as an very effective vehicle to disseminate throughout the host body or the site of long-term T. gondii persistence, respectively.
Apoptosis is a genetically controlled mechanism of cell death involved in the regulation of tissue homeostasis. The aim of this study was to investigate the influence of Borrelia afzelii, Coxiella burnetii, and Bartonella henselae bacteria on apoptosis measured as the level of caspase 3 activity in human fibroblast cells HEL-299. Our findings show that C. burnetii bacteria may inhibit the process of apoptosis in the host cells for a long time. This can permit intracellular survival in the host and mediatingthe development of chronic disease.
In the present paper we focused on the potential role of human lactoferrin for the intracellular replication rate of T. gondii BK tachyzoites following our earlier observation that Toxoplasma gondii was able to bind human lactoferrin but not serum transferrin. The study was performed in vitro on human CaCo-2 epithelial cells and mouse L929 fibroblasts. We found that the multiplication of the parasite was inhibited by lactoferrin in both cell lines used. However, the direct cytotoxic effect on the parasite and the host cells was not observed. The intracellular growth of T. gondii was not affected when tachyzoites or host cells were only pre-coated with human lactoferrin. The results suggest that lactoferrin does not influence parasites penetration into host cells but could trigger unknown antiparasitic mechanisms in the infected cells.
Listeria monocytogenes, a food-borne intracellular animal and human pathogen, interacts with infected host cells both prior to entry and during the intracellular phase of infection. This review is focused on the role of secreted proteins including listeriolysin O and two distinct phospholipases C, in modulating the signal transduction of infected cells.
Listeria monocytogenes enters non-phagocytic cells by binding its surface proteins inlA (internalin) and inlB to the host’s E-cadherin and Met, respectively. The two internalins play either separate or cooperative roles in the colonization of infected tissues. Here, we studied bacterial uptake into HeLa cells using an L. monocytogenes mutant strain (ΔinlA) carrying a deletion in the gene coding for inlA. The ΔinlA mutant strain showed the capability to invade HeLa cells. The monoclonal anti-β3- and anti-β1-integrin subunit antibodies prevented bacterial uptake into the cells, while the anti-β2- and anti-β4-integrin subunit antibodies failed to affect L. monocytogenes entry into HeLa cells. Three structurally distinct disintegrins (kistrin, echistatin and flavoridin) also inhibited bacterial uptake, showing different potencies correlated to their selective affinity for the β3- and β1-integrin subunits. In addition to inducing Met phosphorylation, infection of cells by the L. monocytogenes ΔinlA mutant strain promoted the tyrosine phosphorylation of the focal adhesion-associated proteins FAK and paxillin. Our findings provide the first evidence that β3- and β1-integrin receptors play a role in the inlB-dependent internalization of L. monocytogenes into host cells.
Microbial colonization is an important step in establishing pathogenic or probiotic relations to host cells and in biofilm formation on industrial or medical devices. The aim of this work was to verify the applicability of quantitative PCR (Real-Time PCR) to measure bacterial colonization of epithelial cells. Salmonella enterica and Caco-2 intestinal epithelial cell line was used as a model. To verify sensitivity of the assay a competition of the pathogen cells to probiotic microorganism was tested. The qPCR method was compared to plate count and radiolabel approach, which are well established techniques in this area of research. The three methods returned similar results. The best quantification accuracy had radiolabel method, followed by qPCR. The plate count results showed coefficient of variation two-times higher than this of qPCR. The quantitative PCR proved to be a reliable method for enumeration of microbes in colonization assay. It has several advantages that make it very useful in case of analyzing mixed populations, where several different species or even strains can be monitored at the same time.
Neospora caninum negatively impacts bovine reproductive performance around the world. Addressing this problem requires a greater understanding of the parasite’s molecular biology. In this study, monoclonal antibodies against recombinant proteins were successfully developed and employed to characterise two different proteins of N. caninum: the acute phase-associated NcGRA7 and the chronic phase-associated NcSAG4. Immunofluorescence with the anti-rNcGRA7 monoclonal antibody suggested that NcGRA7 trafficks from tachyzoite dense granules to the matrix of the parasitophorous vacuole and parasite’s surroundings. Furthermore, NcGRA7 is also expressed in the bradyzoite stage and localised on the matrix of bradyzoite-positive vacuoles. NcGRA7 appears to be partially involved in the tachyzoite-invasion mechanisms, as an anti-rNcGRA7 monoclonal antibody partially inhibited in vitro tachyzoite-invasion. A monoclonal antibody specific for NcSAG4 confirmed this protein’s bradyzoitespecific expression both by western blot and immunofluorescence. However, some bradyzoite-positive vacuoles only weakly expressed NcSAG4, if it was expressed at all. The specificity of the anti-rNcSAG4 monoclonal antibody was confirmed by the recognition of the NcSAG4 in the membrane surface of Nc-1SAG4c transgenic tachyzoites, which constitutively expresses NcSAG4. Blocking NcSAG4 of Nc-1SAG4c tachyzoites with the monoclonal antibody did not affect host cell invasion. However, its implication on the host cell adhesion or host immune evasion should not be discarded.
The prevalence of fungi from the genus Candida in humans is increasing, but the mere fact of their detection does not allow, in general, to diagnose a disease. In fact the development of fungal infection depends on several factors of the host-pathogen relationship. The occurrence of symptoms and the course of the disease are associated, inter alia, with general and immunological conditions of an infected person as well as the properties of strains. Differences between the strains responsible for asymptomatic and symptomatic invasion have been shown. Thus the determination of their pathogenicity parameters is an important element leading to proper identification, both mycological and clinical, which allows for the implementation of therapeutic intervention. There are several virulence factors that are essential for surviving in host’s organism and play important role in each phase of fungal infection. This review provides an update on selected pathogenicity features: formation of hyphae and/or pseudohyphae, phenotypic switching, tropic reactions and biofilm production.
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