High osmotic pressure forPneumocystic carinii London Resin White embedding enables fine immunocytochemistry studies: I. Golgi complex and cell-wall synthesis

Palluault, F; Soulez, B; Slomianny, Christian; Dei‐Cas, Eduardo; Cesbron, Jean Yves; Camus, Daniel

doi:10.1007/bf00931568

Cited by 9 publications

(14 citation statements)

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“…Lesions, which had been identified macroscopically at the ileo-caecal region of mice infected with C. parvum and at the antropyloric region of mice that had been infected with C. parvum or C. muris , were fixed and embedded in EPON using glutaraldehyde 2.5% solution and then washed in PBS (0.1 M, pH 7.4) to optimize the preservation of cell structures (Aliouat et al, 1995; Palluault et al, 1992). Ultrathin sections were contrasted with uranyl acetate and lead citrate, and examined using a transmission electron microscope (LEO-906, Leica, Rueil-Malmaison, France).…”

Section: Methodsmentioning

confidence: 99%

Cryptosporidium parvum-induced ileo-caecal adenocarcinoma and WNT signaling in a rodent model

Benamrouz

Conseil

Chabé

et al. 2014

Disease Models &Amp; Mechanisms

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Cryptosporidium species are apicomplexan protozoans that are found worldwide. These parasites constitute a large risk to human and animal health. They cause self-limited diarrhea in immunocompetent hosts and a life-threatening disease in immunocompromised hosts. Interestingly, Cryptosporidium parvum has been related to digestive carcinogenesis in humans. Consistent with a potential tumorigenic role of this parasite, in an original reproducible animal model of chronic cryptosporidiosis based on dexamethasone-treated or untreated adult SCID mice, we formerly reported that C. parvum (strains of animal and human origin) is able to induce digestive adenocarcinoma even in infections induced with very low inoculum. The aim of this study was to further characterize this animal model and to explore metabolic pathways potentially involved in the development of C. parvum-induced ileo-caecal oncogenesis. We searched for alterations in genes or proteins commonly involved in cell cycle, differentiation or cell migration, such as β-catenin, Apc, E-cadherin, Kras and p53. After infection of animals with C. parvum we demonstrated immunohistochemical abnormal localization of Wnt signaling pathway components and p53. Mutations in the selected loci of studied genes were not found after high-throughput sequencing. Furthermore, alterations in the ultrastructure of adherens junctions of the ileo-caecal neoplastic epithelia of C. parvum-infected mice were recorded using transmission electron microscopy. In conclusion, we found for the first time that the Wnt signaling pathway, and particularly the cytoskeleton network, seems to be pivotal for the development of the C. parvum-induced neoplastic process and cell migration of transformed cells. Furthermore, this model is a valuable tool in understanding the host-pathogen interactions associated with the intricate infection process of this parasite, which is able to modulate host cytoskeleton activities and several host-cell biological processes and remains a significant cause of infection worldwide.

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Section: Methodsmentioning

confidence: 99%

Cryptosporidium parvum-induced ileo-caecal adenocarcinoma and WNT signaling in a rodent model

Benamrouz

Conseil

Chabé

et al. 2014

Disease Models &Amp; Mechanisms

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“…CONCLUSION Meaningful advances in the ultrastructure of Pneumocystis organisms have been made. Typical cytoplasmic organelles of eukaryotic cells have been found and described in the parasite (53,54,55,58,59). In contrast, the cyst wall shows an outer membrane, which seems similar to the outer membrane described in prokaryote organisms (23).…”

Section: Is Pneumocystosis a Fungal Disease?mentioning

confidence: 94%

“…carinii cyst wall to CortA is considered strong (16, 91) the authors overlook the fact that lectin concentration used to label the cell wall of C. albicans is about 20 times as low as the lectin concentration needed to label the P. carinii cyst wall (53,91). Comparative evaluation attempts should also take into account the fact that endogenous biotin could be present in the P. carinii cytoplasm and be directly labelled by streptavidin conjugates (53,59). Furthermore, streptavidin contains a RYD sequence which mimics the RGD receptor domain of fibronectin (3): this may also be important as it was shown that gp120, a major constitutive surface P. carinii antigen, functions as a fibronectin binding protein (63).…”

Section: Is Pneumocystis Carinii a Fungus?mentioning

confidence: 99%

“…The biological relevance of these ultrastructural results, summarized below, may be given by the fact that up to 1989-90, neither Golgi complex nor lysosomal system had been observed in any stage of P. carinii. On the one hand, improvements were performed in methods to prepare P. carinii samples for ultrastructural study (32,58,59). On the other hand, cytochemistry, serial sectioning and three-dimensional reconstruction methods were applied to the ultrastructural study of the parasite (53, 54, 55, 56).…”

Section: Other Organellesmentioning

confidence: 99%

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Is Pneumocystis carinii a deep mycosis-like agent?

et al. 1992

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Pneumocystis carinii is a widespread eukaryotic microorganism found in the lungs of healthy mammals, including humans. It is able to proliferate extensively in the alveoli, becoming an important agent of severe pneumonitis in immunosuppressed hosts, especially in persons suffering from AIDS. The taxonomic position of P. carinii is uncertain. Typical cytoplasmic organelles of eukaryotic cells have been found and described in the parasite. Biochemical research is hindered by the lack of an efficient in vitro culture system. Results of comparative study of nucleic acid sequences suggest that Pneumocystis is a fungus. However, ultrastructural, biochemical and nucleic acid homology insights appear as clearly insufficient to class Pneumocystis. Pneumocystis infection might be acquired, as deep mycoses, from environmental sources through the respiratory tract. Thus, the hypothesis of an environmental stage of the parasite must be considered. Pneumocystis might be seen as a widespread pathogenic dimorphous fungus. As fungal agents, P. carinii is able to disseminate from the infected lung to other organs. However, deep mycoses and pneumocystosis induce different histopathological changes in the host. Furthermore, deep fungal infections, unlike pneumocystosis, cannot be transmitted from one infested host to another one. Beside these two aspects, pneumocystosis shares many features with deep mycoses. Research on the epidemiology of pneumocystosis is needed.

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“…Most knowledge about rabbit‐derived Pneumocystis cell structure resulted from studies made in the 1990s thanks to both significant improvements of TEM‐fixation methods (Palluault et al , 1992a, b), and computer‐aided 3D reconstruction studies (Palluault et al , 1991a, b, c). Interestingly, these studies revealed distinctive ultrastructural features of rabbit Pneumocystis (Dei‐Cas et al , 1994; Mazars & Dei‐Cas, 1998; Nielsen et al , 1998; Durand‐Joly et al , 2000).…”

Section: Pneumocystis and Pneumocystosis In Rabbitsmentioning

confidence: 99%

Pneumocystis oryctolagisp. nov., an uncultured fungus causing pneumonia in rabbits at weaning: review of current knowledge, and description of a new taxon on genotypic, phylogenetic and phenotypic bases

et al. 2006

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The genus Pneumocystis comprises noncultivable, highly diversified fungal pathogens dwelling in the lungs of mammals. The genus includes numerous host-species-specific species that are able to induce severe pneumonitis, especially in severely immunocompromised hosts. Pneumocystis organisms attach specifically to type-1 epithelial alveolar cells, showing a high level of subtle and efficient adaptation to the alveolar microenvironment. Pneumocystis species show little difference at the light microscopy level but DNA sequences of Pneumocystis from humans, other primates, rodents, rabbits, insectivores and other mammals present a host-species-related marked divergence. Consistently, selective infectivity could be proven by cross-infection experiments. Furthermore, phylogeny among primate Pneumocystis species was correlated with the phylogeny of their hosts. This observation suggested that cophylogeny could explain both the current distribution of pathogens in their hosts and the speciation. Thus, molecular, ultrastructural and biological differences among organisms from different mammals strengthen the view of multiple species existing within the genus Pneumocystis. The following species were subsequently described: Pneumocystis jirovecii in humans, Pneumocystis carinii and Pneumocystis wakefieldiae in rats, and Pneumocystis murina in mice. The present work focuses on Pneumocystis oryctolagi sp. nov. from Old-World rabbits. This new species has been described on the basis of both biological and phylogenetic species concepts.

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High osmotic pressure forPneumocystic carinii London Resin White embedding enables fine immunocytochemistry studies: I. Golgi complex and cell-wall synthesis

Cited by 9 publications

References 14 publications

Cryptosporidium parvum-induced ileo-caecal adenocarcinoma and WNT signaling in a rodent model

Cryptosporidium parvum-induced ileo-caecal adenocarcinoma and WNT signaling in a rodent model

Is Pneumocystis carinii a deep mycosis-like agent?

Pneumocystis oryctolagisp. nov., an uncultured fungus causing pneumonia in rabbits at weaning: review of current knowledge, and description of a new taxon on genotypic, phylogenetic and phenotypic bases

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