Invasion von Erythrozyten durch Toxoplasma gondii

Schupp, E.; Michel, R.; Raether, W.; Niemeitz, H.; Uphoff, M.

doi:10.1007/bf00390369

Cited by 12 publications

(4 citation statements)

References 6 publications

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“…Host-cell entry by haemosporidan and coccidian parasites, such as Plasmodium zoites (sporozoites and merozoites) or Toxoplasma gondii tachyzoites, is defined by the formation of a specialised tight or moving junction (reviewed in [5]). By electron microscopy (EM) this structure appears as a circular electron dense interface that forms between the parasite and host cell during entry and constitutes an aperture through which the parasite passes en route to intracellular infection [6], [7]. The junction functions as an intersection around which the key events for invasion are organised [8].…”

Section: Introductionmentioning

confidence: 99%

Subcompartmentalisation of Proteins in the Rhoptries Correlates with Ordered Events of Erythrocyte Invasion by the Blood Stage Malaria Parasite

et al. 2012

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Host cell infection by apicomplexan parasites plays an essential role in lifecycle progression for these obligate intracellular pathogens. For most species, including the etiological agents of malaria and toxoplasmosis, infection requires active host-cell invasion dependent on formation of a tight junction – the organising interface between parasite and host cell during entry. Formation of this structure is not, however, shared across all Apicomplexa or indeed all parasite lifecycle stages. Here, using an in silico integrative genomic search and endogenous gene-tagging strategy, we sought to characterise proteins that function specifically during junction-dependent invasion, a class of proteins we term invasins to distinguish them from adhesins that function in species specific host-cell recognition. High-definition imaging of tagged Plasmodium falciparum invasins localised proteins to multiple cellular compartments of the blood stage merozoite. This includes several that localise to distinct subcompartments within the rhoptries. While originating from the same organelle, however, each has very different dynamics during invasion. Apical Sushi Protein and Rhoptry Neck protein 2 release early, following the junction, whilst a novel rhoptry protein PFF0645c releases only after invasion is complete. This supports the idea that organisation of proteins within a secretory organelle determines the order and destination of protein secretion and provides a localisation-based classification strategy for predicting invasin function during apicomplexan parasite invasion.

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Section: Introductionmentioning

confidence: 99%

Subcompartmentalisation of Proteins in the Rhoptries Correlates with Ordered Events of Erythrocyte Invasion by the Blood Stage Malaria Parasite

et al. 2012

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“…No animal cell type, probably including erythrocytes (Schupp et al, 1978), has been found to be resistant to Toxoplasma invasion. However, different degrees of susceptibility of host cells to infection have been reported, due either to the type of target cell (Tanabe et al, 1979) or to modification of the membrane microviscosity by chemical factors, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…It can thus be concluded that plant protoplasts are the only cell type so far found to be totally resistant to Toxoplasma gondii infection; invasion of mature erythrocytes as reported by Schupp et al (1978) is still a matter of controversy (Tanabe et al, 1979). Further studies are necessary to analyse the mechanism of resistance of plant protoplasts to infection with Toxoplasma gondii, and these may throw light on the factors required for infection of susceptible cells.…”

Section: Discussionmentioning

confidence: 99%

Attempts to Infect Plant Protoplasts with Toxoplasma gondii

Werk

Fischer

1982

Microbiology

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211The interaction of tachyzoites of Toxoplasma gondii with plant protoplasts was compared with their interaction with cultures of HeLa cells. Unlike the HeLa cells, the plant protoplasts were refractory to invasion under all conditions tested. The lack of invasion was not an artefact of the protoplast isolation technique. This is the first description of a cell type refractory to Toxoplasma invasion; hence possible mechanisms for the specificity of parasite-host cell interaction can now be studied. I N T R O D U C T I O NToxoplasma gondii infects an unusually broad range of host cells: it will infect cells of vertebrates (Doran, 1973), including those of fish (S. Takada, personal communication), as well as insect cells (Buckley, 1973). So far, no cell type totally resistant to Toxoplasma gondii infection has been reported. The discovery of a cell line resistant to infection might introduce new aspects on Toxoplasma gondii invasion. An experimental model using plant protoplasts as target cells for Toxoplasma parasites is described in this paper. Plant protoplasts were chosen since they differ from animal cells in fine structure and composition of the membrane, including the cell surface (Evans, 1976). M E T H O D SOrganisms. Toxoplasma parasites were isolated from the peritoneal cavity of mice as described previously (Werk & Bommer, 1978). Candida albicans cultures were obtained from the mould culture collection of the Institut fur Hygiene und Medizinische Mikrobiologie der Universitat Wurzburg (Professor Seeliger).Cell and protoplast cultures. Cover-slip cultures of HeLa cells were prepared according to Werk & Bommer (1 980).Plant protoplasts were prepared as follows. Young leaves of Cafharanfhus roseus (Apocynaceae) and Brassica napus napus (Brassicaceae) were sterilized for 10 s in 70% (v/v) ethanol and then for 30 min in 5 % (v/v) sodium hypochlorite solution. After washing three times with deionized water, the leaves were cut into small pieces and left in 0.55 ~-mannitol for 30 min at room temperature to let cell debris settle. The leaf material was incubated in Erlenmeyer flasks for about 14 h at 22 "C with a cell wall digestion mixture containing 0.4%) (w/v) Cellulase 'Onozuka' RlO, 0.1% Mazerozyme R10 (both enzymes from Kinki Yakult, Nishinomiya, Japan) and 79.3 yM-Ca(H,PO,),, in 0.55 M-mannitol adjusted to pH 7-0 with KOH. Protoplasts were then obtained by shaking the flasks for 30 min. The protoplast suspension was passed sequentially through two nylon meshes (mesh size 125 and 40 pm) and collected by centrifugation (200g, 10 min). The procedure was repeated three or four times and the enzyme solution was replaced by 0.55 M-mannitol or a modified protoplast culture medium (Nitsch & Nitsch, 1969) containing 9.1 % (w/v) mannitol, 10% (w/v) glucose and 20% (w/v) sucrose.Infection studies. The experimental schedule, which also indicates the ratio of host 'target' cells to parasite cells, is described in Table 1. Host cells were presented to Toxoplasma either in 0.55 M-rnannitOI or in plant protoplast cultu...

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“…T. gondii has been found to replicate in chicken macrophages, suggesting their importance in activating host immune responses during infection [9,10]. Furthermore, erythrocytes from various host species have been confirmed to be infected by tachyzoites [11,12]; therefore, T. gondii may have a high possibility of invading nucleated cell populations in chicken erythrocytes, promoting its dissemination in avian hosts. It is well known that chicken erythrocytes express toll-like receptors and cytokines in response to pathogen infection.…”

Section: Introductionmentioning

confidence: 99%

Toxoplasma gondii Adhesion and Apoptosis of Chicken Erythrocytes

Zhang

Sang

et al. 2023

Preprint

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Background: Toxoplasma gondii (T. gondii) was thought to infect all nucleated cells in warm-blooded animals, including poultry, mammals, and humans. However, it is unclear whether T. gondii can infect chicken erythrocytes due to the nucleated nature of these cells. Due to the special role of chicken erythrocytes in innate immunity, we investigated the cell-cell interaction between T. gondii and erythrocytes to elucidate the role of chicken erythrocytes in T. gondii infection. Methods: Cellular apoptosis was analyzed by transwell assay and flow cytometry. An immunofluorescence method was used to examine the reorganization of vimentin during T. gondii infection in both Vero cells and chicken erythrocytes. The reorganization of actin was evaluated to further examine the invasion capacity of tachyzoites on chicken erythrocytes during infection. The transcriptional levels of virulence factors ROP18, ROP16, and MIC3 were calculated using the real-time PCR method to determine whether T. gondii virulence was reduced when co-cultured with chicken erythrocytes. Results: We discovered that T. gondii can adhere to but not invade chicken erythrocytes and eventually cause apoptosis in chicken erythrocytes. When tachyzoites were co-cultured with chicken erythrocytes in vitro, the transcriptional levels of T. gondii MIC3, ROP16, and ROP18 were significantly decreased. In addition, the rearrangement of host cell vimentin, a type III cytoskeleton protein regulated by T. gondii infection, was not observed. Similarly, the parasite-induced ring-shaped actin structure was not expressed and formed in the host-parasite junction. T. gondii RH tachyzoites preferentially invaded Vero cells and replicated in chicken blood monocytes, but they were not found in chicken erythrocytes. These findings showed that although T. gondii can attach to the surface of chicken erythrocytes, it’s unable to invade successfully, showing an inability to invade. Interestingly, we found that T. gondii secretome, lysates, and intact tachyzoites could cause apoptosis of chicken erythrocytes to varying degrees, which suggested a complex mechanism involved in the apoptosis of chicken erythrocytes induced by T. gondii. Conclusions: This study elucidated that T. gondii can’t infect nucleated chicken erythrocytes and enriched our understanding of T. gondii's transmission mechanism among avian species.

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Invasion von Erythrozyten durch Toxoplasma gondii

Abstract: The in vitro-invasion of mouse erythrocytes by Toxoplasma gondii could be detected and analysed by electron microscopy. The sequence of events observed during erythrocyte invasion led to the assumption of an actively penetrating parasite into the non-phagocytic host cell.

Cited by 12 publications

References 6 publications

Subcompartmentalisation of Proteins in the Rhoptries Correlates with Ordered Events of Erythrocyte Invasion by the Blood Stage Malaria Parasite

Subcompartmentalisation of Proteins in the Rhoptries Correlates with Ordered Events of Erythrocyte Invasion by the Blood Stage Malaria Parasite

Attempts to Infect Plant Protoplasts with Toxoplasma gondii

Toxoplasma gondii Adhesion and Apoptosis of Chicken Erythrocytes

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