Relevant bibliographies by topics / Intracellular vacuoles

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Academic literature on the topic 'Intracellular vacuoles'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Intracellular vacuoles"

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Baintner, K. "Demonstration of acidity in intestinal vacuoles of the suckling rat and pig." Journal of Histochemistry & Cytochemistry 42, no. 2 (February 1994): 231–38. http://dx.doi.org/10.1177/42.2.7507141.

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Fluorescence staining characteristics of "large vacuoles," i.e. vacuoles ranging up to almost cell size, were studied in suckling rats and pigs. In the distal epithelium of the small intestine of suckling rat, yellow autofluorescence and accumulation of orally administered FITC-dextran were observed in the supranuclear vacuole. In both species the weakly basic amino dye acridine orange (AO) stained the nuclei at neutral pH bright yellow-green and the transport and digestive vacuoles bright red or orange. It is concluded that trapping and accumulation of the dye (red shift) were due to the acidity of the vacuolar interior. Assessment of the vacuolar pH in rat enterocytes is in agreement with published data on lysosomal pH values. Acidic buffers, lysosomotropic and destructive agents, or illumination with bright light induced irreversible fading of AO-stained vacuoles; the color of the porcine transport vacuoles was the most labile. This fading was used to differentiate vacuoles from other structures, e.g., vacuolar inclusion bodies and goblet cells. In suckling rat, staining characteristics of the gut epithelium changed on Days 19 and 20 of postnatal age. Detection of acidity in the distal (digestive) vacuoles supports the lysosome-like nature of their function. They appear to constitute an auxiliary, intracellular digestive system for the young animal. However, the function of acidity in the non-digestive transport vacuoles of newborn pig is unclear.
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Gedde, Margaret M., Darren E. Higgins, Lewis G. Tilney, and Daniel A. Portnoy. "Role of Listeriolysin O in Cell-to-Cell Spread ofListeria monocytogenes." Infection and Immunity 68, no. 2 (February 1, 2000): 999–1003. http://dx.doi.org/10.1128/iai.68.2.999-1003.2000.

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ABSTRACT Listeria monocytogenes is a facultative intracellular bacterial pathogen that escapes from a host vacuolar compartment and grows rapidly in the cytosol. Listeriolysin O (LLO) is a secreted pore-forming protein essential for the escape of L. monocytogenes from the vacuole formed upon initial internalization. However, its role in intracellular growth and cell-to-cell spread events has not been testable by a genetic approach. In this study, purified six-His-tagged LLO (HisLLO) was noncovalently coupled to the surface of nickel-treated LLO-negative mutants. Bound LLO mediated vacuolar escape in approximately 2% of the mutants. After 5.5 h of growth, cytosolic bacteria were indistinguishable from wild-type bacteria with regard to formation of pseudopod-like extensions, here termed listeriopods, and spread to adjacent cells. However, bacteria in adjacent cells failed to multiply and were found in double-membrane vacuoles. Addition of bound LLO to mutants lacking LLO and two distinct phospholipases C (PLCs) also resulted in spread to adjacent cells, but these triple mutants became trapped in multiple-membrane vacuoles that are reminiscent of autophagocytic vacuoles. These studies show that neither LLO nor the PLCs are necessary for listeriopod formation and uptake of bacteria into neighboring cells but that LLO is required for the escape ofL. monocytogenes from the double-membrane vacuole that forms upon cell-to-cell spread.
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Tan, Xiaona, Kaixia Li, Zheng Wang, Keming Zhu, Xiaoli Tan, and Jun Cao. "A Review of Plant Vacuoles: Formation, Located Proteins, and Functions." Plants 8, no. 9 (September 5, 2019): 327. http://dx.doi.org/10.3390/plants8090327.

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Vacuoles, cellular membrane-bound organelles, are the largest compartments of cells, occupying up to 90% of the volume of plant cells. Vacuoles are formed by the biosynthetic and endocytotic pathways. In plants, the vacuole is crucial for growth and development and has a variety of functions, including storage and transport, intracellular environmental stability, and response to injury. Depending on the cell type and growth conditions, the size of vacuoles is highly dynamic. Different types of cell vacuoles store different substances, such as alkaloids, protein enzymes, inorganic salts, sugars, etc., and play important roles in multiple signaling pathways. Here, we summarize vacuole formation, types, vacuole-located proteins, and functions.
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Shepherd, V. A., D. A. Orlovich, and A. E. Ashford. "A dynamic continuum of pleiomorphic tubules and vacuoles in growing hyphae of a fungus." Journal of Cell Science 104, no. 2 (February 1, 1993): 495–507. http://dx.doi.org/10.1242/jcs.104.2.495.

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The vacuole system in growing hyphal tips of Pisolithus tinctorius is a dynamic continuum of vacuoles and extensible tubular elements. The system varies from a tubular reticulum with few vacuoles across a spectrum of intermediate forms to clusters of vacuoles with few tubules. Spherical vacuoles interconnected in clusters are situated at intervals along the hyphal tip and are transiently linked by tubules that extend from a vacuole in one cluster and fuse with that of another. Extension and retraction of the tubules is independent of cytoplasmic streaming, can occur in either direction, and covers distances as great as 60 micrometre. The tubules pulsate and peristalsis-like movements transfer globules of material along them between the vacuoles in different clusters. The tubules also generate vacuoles. The tubular system has the potential for intracellular transport of solutes in the hyphal tips without concomitant transfer of large amounts of membrane. This contrasts with models of intracellular transport via vesicles, where the ratio of membrane transferred to internal content is very much higher. The system has many features in common with tubular endosomal and lysosomal systems in cultured animal cells.
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Sauer, John-Demian, Jeffrey G. Shannon, Dale Howe, Stanley F. Hayes, Michele S. Swanson, and Robert A. Heinzen. "Specificity of Legionella pneumophila and Coxiella burnetii Vacuoles and Versatility of Legionella pneumophila Revealed by Coinfection." Infection and Immunity 73, no. 8 (August 2005): 4494–504. http://dx.doi.org/10.1128/iai.73.8.4494-4504.2005.

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ABSTRACT Legionella pneumophila and Coxiella burnetii are phylogenetically related intracellular bacteria that cause aerosol-transmitted lung infections. In host cells both pathogens proliferate in vacuoles whose biogenesis displays some common features. To test the functional similarity of their respective intracellular niches, African green monkey kidney epithelial (Vero) cells, A/J mouse bone marrow-derived macrophages, human macrophages, and human dendritic cells (DC) containing mature C. burnetii replication vacuoles were superinfected with L. pneumophila, and then the acidity, lysosome-associated membrane protein (LAMP) content, and cohabitation of mature replication vacuoles was assessed. In all cell types, wild-type L. pneumophila occupied distinct vacuoles in close association with acidic, LAMP-positive C. burnetii replication vacuoles. In murine macrophages, but not primate macrophages, DC, or epithelial cells, L. pneumophila replication vacuoles were acidic and LAMP positive. Unlike wild-type L. pneumophila, type IV secretion-deficient dotA mutants trafficked to lysosome-like C. burnetii vacuoles in Vero cells where they survived but failed to replicate. In primate macrophages, DC, or epithelial cells, growth of L. pneumophila was as robust in superinfected cell cultures as in those singly infected. Thus, despite their noted similarities, L. pneumophila and C. burnetii are exquisitely adapted for replication in unique replication vacuoles, and factors that maintain the C. burnetii replication vacuole do not alter biogenesis of an adjacent L. pneumophila replication vacuole. Moreover, L. pneumophila can replicate efficiently in either lysosomal vacuoles of A/J mouse cells or in nonlysosomal vacuoles of primate cells.
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Kim, Donghyeun, Moonyong Song, Eunsoo Do, Yoojeong Choi, James W. Kronstad, and Won Hee Jung. "Oxidative Stress Causes Vacuolar Fragmentation in the Human Fungal Pathogen Cryptococcus neoformans." Journal of Fungi 7, no. 7 (June 29, 2021): 523. http://dx.doi.org/10.3390/jof7070523.

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Vacuoles are dynamic cellular organelles, and their morphology is altered by various stimuli or stresses. Vacuoles play an important role in the physiology and virulence of many fungal pathogens. For example, a Cryptococcus neoformans mutant deficient in vacuolar functions showed significantly reduced expression of virulence factors such as capsule and melanin synthesis and was avirulent in a mouse model of cryptococcosis. In the current study, we found significantly increased vacuolar fragmentation in the C. neoformans mutants lacking SOD1 or SOD2, which respectively encode Zn, Cu-superoxide dismutase and Mn-superoxide dismutase. The sod2 mutant showed a greater level of vacuole fragmentation than the sod1 mutant. We also observed that the vacuoles were highly fragmented when wild-type cells were grown in a medium containing high concentrations of iron, copper, or zinc. Moreover, elevated temperature and treatment with the antifungal drug fluconazole caused increased vacuolar fragmentation. These conditions also commonly cause an increase in the levels of intracellular reactive oxygen species in the fungus, suggesting that vacuoles are fragmented in response to oxidative stress. Furthermore, we observed that Sod2 is not only localized in mitochondria but also in the cytoplasm within phagocytosed C. neoformans cells, possibly due to copper or iron limitation.
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Dorn, Brian R., William A. Dunn, and Ann Progulske-Fox. "Porphyromonas gingivalis Traffics to Autophagosomes in Human Coronary Artery Endothelial Cells." Infection and Immunity 69, no. 9 (September 1, 2001): 5698–708. http://dx.doi.org/10.1128/iai.69.9.5698-5708.2001.

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ABSTRACT Porphyromonas gingivalis is a periodontal pathogen that also localizes to atherosclerotic plaques. Our previous studies demonstrated that P. gingivalis is capable of invading endothelial cells and that intracellular bacteria are contained in vacuoles that resemble autophagosomes. In this study, we have examined the trafficking of P. gingivalis 381 to the autophagic pathway. P. gingivalis 381 internalized by human coronary artery endothelial (HCAE) cells is located within vacuoles morphologically identical to autophagosomes. The progression ofP. gingivalis 381 through intracellular vacuoles was analyzed by immunofluorescence microscopy. Vacuoles containingP. gingivalis colocalize with Rab5 and HsGsa7p early after internalization. At later times, P. gingivaliscolocalizes with BiP and then progresses to a vacuole that contains BiP and lysosomal glycoprotein 120. Late endosomal markers and the lysosomal cathepsin L do not colocalize with P. gingivalis 381. The intracellular survival of P. gingivalis 381 decreases over 8 h in HCAE cells pretreated with the autophagy inhibitors 3-methyladenine and wortmannin. In addition, the vacuole containing P. gingivalis 381 lacks BiP but contains cathepsin L in the presence of wortmannin. These results suggest that P. gingivalis 381 evades the endocytic pathway to lysosomes and instead traffics to the autophagosome.
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Saito, I., S. Hashimoto, A. Saluja, M. L. Steer, and J. Meldolesi. "Intracellular transport of pancreatic zymogens during caerulein supramaximal stimulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 4 (October 1, 1987): G517—G526. http://dx.doi.org/10.1152/ajpgi.1987.253.4.g517.

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Rats infused with a dose of the secretagogue caerulein that is in excess of that which stimulates a maximal rate of pancreatic digestive enzyme secretion develop acute edematous pancreatitis. We have previously noted that infusion of this dose of caerulein (5 micrograms . kg-1 . h-1) induces the appearance of large heterogeneous vacuoles in acinar cell, blockade of exocytosis, and intracellular accumulation of digestive zymogens [O. Watanabe et al. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G457-G467, 1984 and A. Saluja et al. Am. J. Physiol. 249 (Gastrointest. Liver Physiol. 12): G702-G710, 1985]. The current studies were performed to further elucidate these phenomena at the electron microscopic level of resolution and employed the techniques of pulse labeling, radioautography, and immunolocalization. Rats were infused with caerulein (5 micrograms . kg-1 . h-1) for 1 h, given a pulse of [3H]phenylalanine, and killed at selected times during the subsequent 5- to 180-min postpulse period during which caerulein infusion was continued. Transport from the endoplasmic reticulum to the Golgi cisternae was not altered by supramaximal stimulation, but transport through post-Golgi elements was altered. In particular, the maturation of condensing vacuoles into zymogen granules was found to be impaired. This led to the accumulation of partially condensed vacuoles and to the development of the large vacuoles containing newly synthesized digestive zymogens as well as the lysosomal hydrolase cathepsin D. The source of the latter could be impaired sorting of lysosomal and digestive enzymes and/or fusion of vacuoles with lysosomes. At the later times after pulse labeling, mature zymogen granules were also found to fuse with these large cathepsin D-containing vacuoles by a process analogous to crinophagy. Thus these studies indicate that the large heterogeneous vacuoles that appear during supramaximal secretagogue stimulation and that contain admixed digestive zymogens and lysosomal hydrolases arise by at least two mechanisms, impaired condensing vacuole maturation and crinophagy.
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Kirk, K. L. "Origin of ADH-induced vacuoles in rabbit cortical collecting tubule." American Journal of Physiology-Renal Physiology 254, no. 5 (May 1, 1988): F719—F733. http://dx.doi.org/10.1152/ajprenal.1988.254.5.f719.

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The origin of the vacuoles that form in the mammalian collecting duct during antidiuretic hormone (ADH)-mediated water reabsorption was examined using two computer-assisted, light microscopic methods. First, differential interference-contrast microscopy was used in combination with a simple morphometric procedure to quantitatively characterize the time course, magnitude, and cell specificity of vacuole formation in the microperfused rabbit cortical collecting tubule. Second, video-intensified fluorescence microscopy was used to visualize the basolateral endocytosis of a fluorescent, fluid-phase marker (i.e., lucifer yellow) during vacuole formation. In the presence of a lumen-to-bath osmotic gradient, ADH addition induced the rapid (less than 10 min) formation of large (1- to 3-micron diam) vacuoles in principal cells and, to a lesser extent, in a subpopulation of intercalated cells. The vacuoles subsequently shrank and disappeared over the course of 60-90 min in the continued presence of the hormone and osmotic gradient. The vacuoles collapsed very slowly after elimination of the osmotic gradient at the peak of the vacuolation response, which implies that these structures are intracellular compartments rather than dilated extracellular spaces. During their formation the vacuoles could be loaded with peritubular (but not luminal) lucifer yellow, which remained trapped within most of these structures well after the dye was removed from the bath (greater than 30 min). These results indicate that most vacuoles that form during ADH-mediated water reabsorption are intracellular, endocytic compartments that communicate with the peritubular space via endocytosis of basolateral cell membrane.
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Hardiman, Camille A., Justin A. McDonough, Hayley J. Newton, and Craig R. Roy. "The role of Rab GTPases in the transport of vacuoles containing Legionella pneumophila and Coxiella burnetii." Biochemical Society Transactions 40, no. 6 (November 21, 2012): 1353–59. http://dx.doi.org/10.1042/bst20120167.

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Intracellular pathogens survive in eukaryotic cells by evading a variety of host defences. To avoid degradation through the endocytic pathway, intracellular bacteria must adapt their phagosomes into protective compartments that promote bacterial replication. Legionella pneumophila and Coxiella burnetii are Gram-negative intracellular pathogens that remodel their phagosomes by co-opting components of the host cell, including Rab GTPases. L. pneumophila and C. burnetii are related phylogenetically and share an analogous type IV secretion system for delivering bacterial effectors into the host cell. Some of these effectors mimic eukaryotic biochemical activities to recruit and modify Rabs at the vacuole. In the present review, we cover how these bacterial species, which utilize divergent strategies to establish replicative vacuoles, use translocated proteins to manipulate host Rabs, as well as exploring which Rabs are implicated in vacuolar biogenesis in these two organisms.
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Dissertations / Theses on the topic "Intracellular vacuoles"

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Kern, Beate. "Analysis of Helicobacter pylori VacA-containing vacuoles and VacA intracellular trafficking." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-184058.

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The human pathogen Helicobacter pylori colonizes half of the global population. Residing at the stomach epithelium, it contributes to the development of diseases like gastritis, duodenal and gastric ulcers, and gastric cancer. It has evolved a range of mechanisms to aid in colonization and persistence, manipulating the host immune response to avoid clearance. A major factor in this is the secreted vacuolating cytotoxin VacA which has a variety of effects on host cells. VacA is endocytosed and forms anion-selective channels in the endosome membrane, causing the compartment to swell. The resulting VacA-containing vacuoles (VCVs) can take up most of the cellular cytoplasm. Even though vacuolation is VacA's most prominent and namesake effect, the purpose of the vacuoles is still unknown. VacA exerts influence on the host immune response in various ways, both pro- and anti- inflammatorily. Most importantly, it disrupts calcium signaling in T-lymphocytes, inhibiting T-cell activation and proliferation and thereby suppressing the host immune response. Furthermore, VacA is transported to mitochondria, where it activates the mitochondrial apoptosis pathway. Within the cell, VacA has only been shown to localize to endocytic compartments/VCVs and mitochondria. Considering its diverse effects, however, the existence of other cellular sites of action seems plausible. In this study, the VCV proteome was comprehensively analyzed for the first time in order to investigate VCV function. To this end, three different strategies for VCV purification from T-cells were devised and tested. Eventually, VCVs were successfully isolated via immunomagnetic separation, using a VacA-specific primary antibody and a secondary antibody coupled to magnetic beads. The purified vacuoles were then measured by mass spectrometry, revealing not only proteins of the endocytic system, but also proteins usually localized in other cellular compartments. This apparent recruitment of proteins involved in all kinds of cellular pathways indicates a central function of VCVs in VacA intoxication effects. In a global evaluation, the VCV proteome exhibited an enrichment of proteins implicated in immune response, cell death, and cellular signaling; all of these are processes that VacA is known to influence. One of the individual proteins contained in the sample was STIM1, a calcium sensor normally residing in the endoplasmic reticulum (ER) that is important in store- operated calcium entry (SOCE). This corroborates the findings of a concurrent report, in which VacA severely influenced SOCE and colocalized with STIM1. A direct interaction of STIM1 with VacA was examined in a pull-down assay, but could be neither shown nor excluded. Immunofluorescence experiments conducted in HeLa cells confirmed the presence of VacA in the ER and also found it to traffic to the Golgi apparatus, identifying these two cellular compartments as novel VacA target structures. The exact route of VacA transport remains unclear, but the involvement of both the ER and the Golgi suggests the possibility of retrograde trafficking, analogous to other bacterial toxins like shiga and cholera toxins. In summary, the elucidation of the VCV proteome and the discovery of the ER and the Golgi apparatus as VacA target structures have generated intriguing starting points for future studies. The detection of many proteins implicated in VacA intoxication effects in the VCV proteome leads to the proposal of VCVs as signaling hubs that may coordinate the complex meshwork of VacA effects. Further investigation of individual proteins is expected to help greatly in illuminating this matter.
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Kortebi, Mounia. "Caractérisation d’une phase de persistance intracellulaire du pathogène Listeria monocytogenes." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS477/document.

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Listeria monocytogenes est une bactérie pathogène intracellulaire facultative responsable d’une pathologie grave, la listériose. Si de très nombreux travaux ont permis de caractériser les mécanismes de virulence de cette bactérie, il existe peu de données sur les mécanismes conduisant au portage asymptomatique de L. monocytogenes dans les hôtes mammifères. L’un de ces mécanismes pourrait être une phase de persistance intracellulaire. Lors d’infections prolongées de cellules épithéliales humaines en culture, comme des hépatocytes et des cellules de trophoblastes, L. monocytogenes change de mode de vie intracellulaire. Après la phase active de dissémination de cellule en cellule, les bactéries arrêtent de polymériser l’actine et se retrouvent piégées dans des vacuoles à simple membrane marquées par la protéine endosomale LAMP1. L’objectif de ma thèse était de caractériser ces « Listeria-Containing Vacuoles » (LisCVs). Nous avons montré que les LisCVs sont des compartiments acides, partiellement-dégradatifs, marquées par la protéase lysosomale cathépsine D. Leur formation coïncide avec la disparition du facteur de polymérisation d’actine ActA de la surface bactérienne et la capture des bactéries cytosoliques dépourvues d’actine par des membranes cellulaires. Dans ces compartiments, les bactéries entrent en croissance ralentie ; une sous-population résiste aux stress et peut survivre au-delà de trois jours d’infection. L’utilisation de la gentamicine lors du protocole d’infection n’est pas responsable de la formation des LisCVs. Cependant, cet antibiotique permet la sélection des bactéries vacuolaires, en inhibant spécifiquement la croissance des bactéries cytosoliques. La formation des LisCVs n’est pas spécifique des souches de laboratoire. Toutefois l’efficacité du phénomène pourrait diverger selon les séquençotypes des souches de L. monocytogenes. Les bactéries vacuolaires ont la capacité de sortir des vacuoles et de retourner vers un état motile et réplicatif, après le passage des cellules infectées. Lorsque l’expression du gène actA reste inactive, comme dans les mutants ∆actA, des formes de Listeria vacuolaires persistent dans les cellules hôtes dans un état viable mais non cultivable (VBNC). Ces formes VBNC peuvent être transmises au cours des divisions des cellules hôtes. L’ensemble de ces résultats révèle une nouvelle phase de persistance dans le processus infectieux intracellulaire de L. monocytogenes lors des infections prolongées de certaines cellules épithéliales. Cette propriété pourrait contribuer au portage asymptomatique de ce pathogène dans les tissus épithéliaux, allonger la période d'incubation de la listériose, et rendre les bactéries tolérantes à l’antibiothérapie
Listeria monocytogenes is a facultative intracellular pathogenic bacterium responsible for a serious disease, listeriosis. Although much work has been done to characterize the virulence mechanisms of this bacterium, there is little data on the mechanisms leading to the asymptomatic carriage of L. monocytogenes in mammalian hosts. One of these mechanisms could be a phase of intracellular persistence. During prolonged infections of human epithelial cells in culture, such as hepatocytes and trophoblast cells, L. monocytogenes changes its intracellular lifestyle. After the active phase of cell-to-cell spread, the bacteria stop polymerizing actin and become trapped in single-membrane vacuoles labeled with the endosomal protein LAMP1.The aim of my thesis was to characterize these "Listeria-Containing Vacuoles" (LisCVs). We have shown that LisCVs are acidic, partially degradative compartments, labeled by the lysosomal protease cathepsin D. Their formation coincides with the disappearance of actin polymerization factor ActA from the bacterial surface and the capture of actin-free cytosolic bacteria by cell membranes. In these compartments, bacterial growth is slowed; a subpopulation is resistant to stress and can survive beyond three days of infection. The use of gentamicin during the infection protocol is not responsible for the formation of LisCVs. However, this antibiotic allows selection of vacuolar bacteria, by specifically inhibiting the growth of cytosolic bacteria. The formation of LisCVs is not specific to laboratory strains. However, the efficacy of the phenomenon could diverge according to the sequence types of L. monocytogenes strains. Vacuolar bacteria have the ability to exit the vacuoles and return to a motile and replicative state during the subculture of infected cells. When expression of the actA gene remains inactive, as in ΔactA mutants, vacuolar Listeria forms persist in host cells in a viable but non-culturable (VBNC) state. These VBNC forms can be transmitted during host cell divisions. All these results reveal a new phase of persistence in the intracellular infectious process of L. monocytogenes during prolonged infections of a subset of epithelial cells. This property could contribute to asymptomatic carriage of this pathogen in epithelial tissues, extend the incubation period of listeriosis, and make bacteria tolerant to antibiotic therapy
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Kern, Beate [Verfasser], and Rainer [Akademischer Betreuer] Haas. "Analysis of Helicobacter pylori VacA-containing vacuoles and VacA intracellular trafficking / Beate Kern. Betreuer: Rainer Haas." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1074825454/34.

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Pereira, Camila Serva. "Aderência, invasão e persistência intracelular de estreptococos do grupo B em células epiteliais respiratórias A549." Universidade do Estado do Rio de Janeiro, 2010. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2392.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Estreptococos do grupo B (EGB) comumente colonizam adultos saudáveis, sem sintomas, mas sob certas circunstâncias possui a capacidade de invadir tecidos do hospedeiro, evadir da detecção imunológica e causar doenças invasivas graves. Por conseguinte, os EGB continuam sendo uma das principais causas de mortalidade neonatal, pneumonia, sepse e meningite. Contudo, a patogênese desta infecção ainda está pouco elucidada. O sorotipo V é freqüentemente associado à doença invasiva em mulheres adultas não gestantes e o segundo mais prevalente em mulheres grávidas. O principal objetivo deste trabalho foi estudar a aderência, invasão e persistência intracelular de amostras pertencentes ao sorotipo V (88641-vagina/portador e 90186-sangue/paciente) usando as células epiteliais respiratórias A549. As amostras de EGB demonstraram capacidade de aderir e invadir as células epiteliais A549, mas somente a amostra 90186-sangue apresentou maior invasão quando comparada com a de vagina (P <0.001). Ambas as amostras demonstraram persistência intracelular sem replicação no interior das células A549. Apenas o isolado 90186-sangue sobreviveu dentro das células epiteliais até 24h de incubação (P <0,05). A fusão dos lisossomas das células epiteliais com vacúolos contendo bactérias foi observada em células A549 tratadas com Lyso Tracker Grenn DND-26 para todas as amostras testadas. Nossos dados indicam pela primeira vez que as amostras viáveis do sorotipo V permanecem dentro de vacúolos ácidos epiteliais. Curiosamente, a amostra 90186- sangue induziu vacuolização celular e a amostra 88641-vagina promoveu a morte celular após 7h de incubação. Finalmente, nossos resultados aumentam o nosso conhecimento sobre eventos celulares da fagocitose e da patogênese das doenças invasivas promovidas pelos EGB.
Group B Streptococcus (GBS) commonly colonizes healthy asymptomatic adults, yetunder certain circumstances displays the ability to invade host tissues, evade the immune system and cause serious invasive disease. Consequently, GBS remains the major cause of neonatal pneumonia, sepsis and meningitis. However, the pathogenesis of this infection is poorly understood. The serotype V is frequently associated with invasive diseases in non-pregnant adults and the second most prevalent in pregnant women. The aim of this work was to study the adherence; invasion and persistence intracellular of the GBS serotype V (88641-vagina/carriers and 90186-blood/patient) in epithelial cells A549. All GBS strains showed ability to adhere and invade the epithelial A549 cells, but GBS 90186-blood was more invasive than the vagina isolate (P<0,001). Both strains persisted intracellular, but without replicating into the A549 cells. Only 90186-blood strain survived within epithelial cells even after a 24h incubation (P<0,05). Fusion of epithelial lysosomes with bacteria containing phagocytic vacuoles was observed in A549 cells treated with Lysotracker Grenn DND-26 for all strains tested. Our data indicate for the first time that viable strains of serotype V remain within acidic epithelial vacuoles. Interestingly, the 90186-blood strain induced cellular vacuolization and 88641-vagina strain caused cell death after 7h incubation. Lastly, our results increase our knowledge about cellular events of phagocytosis and pathogeneses of GBS diseases.
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Huang, Bernice. "Anaplasma phagocytophilum remodels its host cell-derived vacuole into a protective niche by redecorating the vacuolar membrane with select Rab GTPases and bacterial proteins." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/280.

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Anaplasma phagocytophilum is an obligate intracellular bacterium that infects neutrophils to cause the emerging tick-transmitted disease, human granulocytic anaplasmosis (HGA). Following entry, the pathogen replicates within a host cell-derived vacuole that fails to mature along the endocytic pathway, does not acidify, and does not fuse with lysosomes. Selective fusogenicity is prototypical of many vacuole-adapted pathogens and has been attributed, at least in part, to pathogen modification of the vacuolar inclusion membrane and/or to selective recruitment or exclusion of host trafficking regulators. As a result, the A. phagocytophilum-occupied vacuolar membrane (AVM) provides a unique interface to study the host-pathogen interactions critical to A. phagocytophilum intracellular survival. Diverse vacuole-adapted pathogens; including Chlamydia, Legionella, and Salmonella; selectively recruit host Rab GTPases to their vacuolar membranes to establish replicative permissive niches within their host cells. Rab GTPases coordinate many aspects of endocytic and exocytic cargo delivery. We determined that the A. phagocytophilum-occupied vacuole (ApV) selectively recruits a subset of fluorescently-tagged Rabs that are predominantly associated with recycling endosomes. Another emerging theme among vacuole-adapted pathogens is the ability to hijack ubiquitin machinery to modulate host cellular processes. Mono- and polyubiquitination differentially dictate the subcellular localization, activity, and fate of protein substrates. Monoubiquitination directs membrane traffic from the plasma membrane to the endosome and has been shown to promote autophagy. We show that monoubiquitinated proteins decorate the AVM during infection of promyelocytic HL-60 cells, endothelial RF/6A cells, and to a lesser extent, embryonic tick ISE6 cells. Importantly, tetracycline treatment concomitantly promotes loss of the recycling endosome-associated GFP-Rabs and ubiquitinated proteins and acquisition of the late endosomal marker, Rab7, and lysosomal marker, LAMP-1, implicating bacterial-derived proteins in the ApV's altered fusogenicity. Therefore, we rationalized that A. phagocytophilum-encoded proteins that associate with the AVM may establish interactions with the host cell that are important for intracellular survival. By focusing on A. phagocytophilum proteins that are induced during host infection, we identified the first two bacterial-encoded proteins -- APH_1387 and APH_0032 -- that modify the AVM. Although functional studies are hindered by the lack of a system to genetically manipulate Anaplasma, the pathobiological roles of APH_1387 and APH_0032 are likely unique, as both proteins exhibit very little or no homology with any previously described protein. APH_1387 and APH_0032 are present at the cytoplasmic face of the AVM, therefore they likely interact with host proteins. We demonstrate that ectopic expression of APH_1387 and APH_0032 inhibits the ApV development in A. phagocytophilum infected cells. The results presented in this dissertation contribute to our understanding of how A. phagocytophilum modifies the vacuolar membrane in which it resides to establish a safe haven and evade lysosomal degradation.
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Llinares, Elisa. "Function, regulation and intracellular trafficking of the vacuolaryeast pq-loop (Ypq) proteins." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209704.

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The cytoplasm of eukaryotic cells contains several membrane-delimited compartments of specific molecular compositions and functions. Among those, the vacuole of fungal cells is often described as an organelle equivalent to the lysosomes of animal cells and the vacuoles of plant cells. These compartments indeed share two similar features: they contain a wide variety of hydrolases and are the most acidic compartments of the cell, which accounts for their key role in the intracellular degradation of macromolecules. In humans, dysfunctions of the lysosomes often give rise to lysosomal related diseases, such as lysosomal storage disorders. These are a class of metabolic disorders caused by the accumulation of non-degraded macromolecules or impaired export of hydrolytic degradation products. Cystinosis is an autosomal recessive disorder (1/200 000 incidence) generally associated with renal dysfunctions. It is caused by the accumulation and crystallization of cystine, the disulfide of cysteine, into the lumen of lysosomes. Cystinosin, the causative gene product of cystinosis, is present at the lysosomal membrane and catalyses the export of cystine from this compartment. The human cystinosin is a member of the Lysosomal Cystine Transporter (LCT) family. LCT proteins are conserved in all eukaryotic species and are defined by the presence of highly conserved PQ-loop motifs.

During this thesis work, we have studied three LCT proteins of the yeast Saccharomyces cerevisiae, named Ypq1, Ypq2 and Ypq3 (Yeast PQ-loop proteins 1, 2 and 3). We first showed that these proteins localize to the vacuolar membrane. We next studied the roles of these proteins, the regulation of their genes and the mechanisms and signals implicated in their delivery to the vacuolar membrane. We also contributed to the functional characterization of a mammalian homologue of yeast Ypq proteins, named rPqlc2.

In the first part of this work, we report that the Ypq proteins are most probably implicated in the export of basic amino acids from the vacuole to the cytosol. More precisely, Ypq2 and Ypq3 behave like vacuolar arginine and lysine exporters, respectively. Interestingly, the mammalian rPqlc2 protein expressed in yeast reaches the vacuolar membrane and functions as an orthologue of the Ypq proteins. Our results also reveal that the expression of the YPQ3 gene is regulated by the Lys14 transcription factor, responsible for the transcriptional activation of the LYS genes encoding enzymes implicated in the biosynthesis of lysine. We have also noted that, in general, the expression of the expression of the YPQ genes is regulated according to the quality of the nitrogen source available in the extracellular medium, eg. YPQ3 is sensitive to the nitrogen catabolite repression regulatory mechanism.

In the last part of this thesis work, we investigated the intracellular trafficking of the Ypq proteins and show that these predominantly reach the vacuolar membrane via the ALP (alkaline phosphatase) pathway due to the presence of a dileucine-based sorting signal in their sequences. Interestingly, a similar mechanism seems responsible for targeting to the yeast vacuole of the mammalian rPqlc2 protein.

Une caractéristique des cellules eucaryotes est leur organisation en compartiment internes délimité par une membrane lipidique, appelé organelles. Ces compartiments intracellulaires présentent une composition lipidique et protéique particulaire conforme à leur identité et fonction. Les lysosomes de cellules de mammifères et la vacuole fongique jouent un rôle clé dans la digestion intracellulaire de macromolécules et de ce fait leurs lumières sont enrichis d’enzymes hydrolytiques nécessaires à cette action. Des disfonctionnements du lysosome peuvent être la conséquence de pathologie chez l’homme, regroupé sous le nom de maladie lysosomale, lié à un à une accumulation de macromolécules non digéré ou un default d’export des produits d’hydrolysé depuis la lumière du lysosome. La cystinose est une maladie autosomale récessive avec une faible fréquence d’incidence (1/200 000) qui regroupe trois formes cliniques :deux formes rénales graves et une forme extra-rénale. Cette maladie est due à une accumulation et cristallisation de cystine dans la lumière du lysosome qui est corrélé à des mutations ponctuelles dans le gène CTNS qui code pour l’exporteur de cystine, la cystinosine. Cette protéine est un membre de la famille LCT (Lysosomal Cystine Transporter) qui possède des représentants chez les cellules animales, végétales et fongiques. Les protéines de la famille possèdent une taille et une topologie prédite similaire (7 segments transmembranaires) et on retrouve aussi au sein de ces protéines deux exemplaires de motifs PQ. Lors de ce travail de thèse nous nous sommes intéressés à trois membres de la famille LCT chez Saccharomyces cerevisiae que nous avons nommé Ypq1, Ypq2 et Ypq3 pour Yeast PQ-loop proteins. Ces protéines n’ayant pas fait l’objet de nombreuses études, nous nous sommes orientés vers une analyse fonctionnelle et transcriptionnelle. De plus, nous avons également étudié les mécanismes et signaux impliqué dans leur adressage vers la vacuole. Finalement, nous avons également inclus dans notre étude un homologue mammalien de ces protéines, rPqlc2.

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Doctorat en Sciences
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Silva, Luis Lamberti Pinto da. "The intracellular targeting of the plant vacuolar sorting receptor - BP80." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434757.

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Haider, Mustafa M. "The intracellular sorting of vacuolar proteins in the yeast Saccharomyces cerevisiae." Thesis, Durham University, 1989. http://etheses.dur.ac.uk/6495/.

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The mechanism of protein sorting to the vacuole in yeast was studied both in vitro and in vivo. A series of experiments were performed to reconstitute transport of carboxypeptidase Y (CPY) from Golgi vesicles to vacuoles. In order to investigate this process, microsomes were purified from sec, pep4-3 mutant strains that accumulate inactive proCPY in the Golgi when incubated at the nonpermissive temperature. These were mixed with purified vacuoles isolated from a mutant lacking CPY activity, but containing active proteinases A and B. Transported proCPY is maturated by these proteinases to active form. Experiments indicate that maturation of CPY is due to the correct transport of proCPY from microsomes to vacuoles because:- Firstly, the reaction is temperature sensitive, requires ATP and is stimulated by the addition of soluble factors (S100). Secondly, the addition of proteinase A and B inhibitors to the reaction mixtures has a negligible effect on the maturation process. Thirdly, disrupting the membranes by the addition of Triton X-100 before addition of the proteinase inhibitors, inhibited the maturation of proCPY. Fourthly, the majority of CPY activity was observed in the sedimented fraction of the reaction mixtures rather than supernatant fractions. Lastly, analysis with western blot shows a clear band of mature CPY only in the sedimented fraction of the reaction mixtures with ATP. This in vitro system will be invaluable in investigating the molecular events of vacuolar biogenesis. For in vivo sorting of proteins to the vacuole, a series of experiments were performed that involved the genetic fusion of the CPY promoter and prepro-sequence of CPY to the bacterial Gus (β-glucuronidase) reporter gene. The Gus gene was expressed in yeast with high efficiency and the results of sub-cellular fractionation indicated that the Gus product was distributed in all cell components. Using a centromeric vector gave similar results but with a lower efficiency of Gus expression. Removal of 90bp from Gus, including Gus initiation codon does not completely inhibit Gus expression either in bacteria or in yeast. Fusion of the shortened Gus with the CPY prepro-fragment and expression in yeast led to the correct sorting of the CPY-Gus hybrid protein to the vacuole. This CPY-Gus fusion is potentially useful in the genetic analysis of mutations defective in vacuolar protein sorting.
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Henry, Thomas. "Physiologie de S. Typhimurium dans l'environnement intracellulaire : la division bactérienne et la modulation des moteurs moléculaires eucaryotes sur la vacuole contenant Salmonella." Aix-Marseille 2, 2005. http://theses.univ-amu.fr.lama.univ-amu.fr/2005AIX22030.pdf.

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Gomord, Véronique. "Contrôle de l'adressage de la sporamine dans la cellule végétale." Rouen, 1994. http://www.theses.fr/1994ROUES054.

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Le système endomembranaire ou système de sécrétion est constitué de compartiments spécifiques et distincts et de vésicules qui assurent le transport entre ces différents compartiments. Les protéines sécrétées, solubles ou membranaires, sont introduites de façon co-traductionnelle dans le réticulum endoplasmique (RE). Du RE, ces protéines sont transportées tout au long du système endomembranaire de sécrétion jusqu'à leur compartiment cible: l'appareil de Golgi, la vacuole le tonoplaste, la membrane plasmique ou le compartiment extracellulaire. Des travaux récents ont permis d'identifier des signaux spécifiques d'adressage et de rétention qui par leur interaction avec des récepteurs, permettent le transport de certaines protéines vers leur localisation finale. Nos travaux font appel aux approches de la biologie cellulaire et moléculaire pour l'étude du transport et de l'adressage des protéines dans le système endomembranaire de sécrétion chez les plantes. Nous avons modifié par mutagénèse dirigée les signaux d'adressage d'une protéine recombinante modèle, la sporamine. De plus nous avons développé un système d'expression stable de ces protéines recombinantes dans des cellules de tabac (nicotiana tabacum CV BY2). Nous avons ainsi obtenu des cellules transgéniques exprimant fortement une même protéine modèle transportée vers la vacuole (sporamine), vers le milieu extracellulaire (dpro-sporamine) ou retenue dans la fraction microsomale (SpoHDEL ou dproHDEL). L'étude de la localisation intracellulaire de SpoHDEL a permis de montrer l'accumulation de cette protéine dans un compartiment présentant une activité IDPase
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Books on the topic "Intracellular vacuoles"

1

Jean-Pierre, Gorvel, ed. Intracellular pathogens in membrane interactions and vacuole biogenesis. Georgetown, Tex: Landes Bioscience, 2004.

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Jean-Pierre, Gorvel, ed. Intracellular pathogens in membrane interactions and vacuole biogenesis. Georgetown, Tex: Landes Bioscience, 2003.

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Jean-Pierre, Gorvel, ed. Intracellular pathogens in membrane interactions and vacuole biogenesis. Georgetown, Tex: Landes Bioscience, 2003.

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Gorvel, Jean-Pierre. Intracellular Pathogens in Membrane Interactions and Vacuole Biogenesis. Springer, 2004.

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Birtles, Richard. Other bacterial diseasesAnaplasmosis, ehrlichiosis and neorickettsiosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0020.

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In 2001, taxonomic reorganization of the bacterial genera Anaplasma, Ehrlichia, Cowdria and Neorickettsia resulted in the transfer of numerous species between these taxa, and the renaming of the transferred species to reflect their new taxonomic position (Dumler et al. 2001). Among the members of these genera, there are four species of established zoonotic importance, which are therefore the subject of this chapter. Two of these species were affected by the changes outlined above.Although these four species possess markedly different ecologies, they share the fundamental biological character of being obligate intracellular bacteria that reside within vacuoles of eukaryotic cells. This lifestyle underlies their fastidious nature in the laboratory and hence our limited knowledge of their biology and pathogenicity. Nonetheless, despite this shortfall, all four are associated with diseases of established or emerging importance: E. chaffeensis provokes human monocytic ehrlichiosis (HME), E. ewingii causes human ewingii ehrlichiosis (HEE), A. phagocytophilum causes human granulocytic anaplasmosis (HGA), N. sennetsu is the agent of sennetsu neorickettsiosis.The first three pathogens are transmitted by hard (ixodid) ticks and are encountered across the temperate zones of the northern hemisphere (and maybe beyond), although the vast majority of human infections caused by them are currently reported in the USA. There, HME and HGA are second only to Lyme disease (caused by Borrelia burgdorferi) in terms of public health significance. Furthermore, given that there is evidence of increasing population sizes and changing distributions for ixodid species (Scharlemann et al. 2008), it is not unreasonable to predict that the infections they transmit will present an increased medical burden in the future. N. sennetsu remains an enigmatic pathogen; case reports remain scarce, but serological surveys suggest high levels of exposure. The widespread consumption of raw fish across east Asia presents specific infection risks to this region, and an increased awareness that sennetsu neorickettsiosis is among the infections that can be acquired from this source is required before its public health importance can be accurately assessed.
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Book chapters on the topic "Intracellular vacuoles"

1

Martinoia, Enrico, Michael J. Schramm, Ulf-Ingo Flügge, and Georg Kaiser. "Intracellular Distribution of Organic and Inorganic Anions in Mesophyll Cells: Transport Mechanisms in the Tonoplast." In Plant Vacuoles, 407–16. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5341-6_53.

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Boller, Th. "Intracellular Transport of Metabolites in Protoplasts: Transport Between Cytosol and Vacuole." In Proceedings in Life Sciences, 76–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70144-3_10.

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Lukacs, Gergely, Ori D. Rotstein, and Sergio Grinstein. "An Overview of Intracellular pH Regulation: Role of Vacuolar H+-ATPases." In Organellar Proton-ATPases, 29–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22265-2_2.

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Nishimura, Yukio, Hideaki Fujita, Keitaro Kato, and Masaru Himeno. "Expression of Rat Cathepsin D cDNA in Saccharomyces Cerevisiae: Intracellular Sorting of Cathepsin D to Yeast Vacuole." In Aspartic Proteinases, 289–92. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1871-6_34.

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Richens, J. "Intracellular klebsiella infections (donovanosis and rhinoscleroma)." In Oxford Textbook of Medicine, 745–48. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.070609_update_001.

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Two rare intracellular species of Klebsiella, a Gram-negative bacillus, cause granulomatous disease in humans that is found in small endemic foci in warm climates, linked to poverty and poor hygiene. Donovanosis—caused by Klebsiella granulomatis (until recently named Calymmatobacterium granulomatis); presumed to be sexually transmitted; presents with genital ulcers or growths, often accompanied by an inguinal ‘pseudobubo’ (granuloma inguinale). Diagnosed by demonstrating Donovan bodies (vacuoles containing capsulated coccoid bacteria) lying within histiocytes in material taken from a typical lesion. Treatment is with azithromycin; surgery may be needed for complications....
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Richens, John, and Nicole Stoesser. "Intracellular klebsiella infections (donovanosis and rhinoscleroma)." In Oxford Textbook of Medicine, edited by Christopher P. Conlon, 1051–54. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0114.

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Two rare intracellular species of Klebsiella, a Gram-negative bacillus, cause granulomatous disease in humans that is found in small endemic foci in warm climates, linked to poverty and poor hygiene. Donovanosis is caused by Klebsiella granulomatis (previously named Calymmatobacterium granulomatis) and is presumed to be sexually transmitted. Presenting with genital ulcers or growths, often accompanied by an inguinal ‘pseudobubo’ (granuloma inguinale), it is diagnosed by demonstrating Donovan bodies (vacuoles containing capsulated coccoid bacteria) lying within histiocytes in material taken from a typical lesion. Treatment is with azithromycin; surgery may be needed for complications. Rhinoscleroma, caused by Klebsiella rhinoscleromatis, is believed to transfer from person to person; following a period of rhinitis it most typically manifests with bulky growths in the upper respiratory tract. It is diagnosed by demonstrating intracellular organisms in typical lesions, combined with culture. Treatment is with ciprofloxacin; surgical debulking of lesions and/or reconstruction may be required.
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Dhamija, Radhika, Erin Conboy, and Lily C. Wong-Kisiel. "Lysosomal Storage Disorders." In Mayo Clinic Neurology Board Review, edited by Kelly D. Flemming, 1106–13. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197512166.003.0121.

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Lysosomes are membrane-bound organelles that degrade various macromolecules. Lysosomal storage diseases are a clinically, enzymatically, and genetically heterogeneous group of disorders resulting from intracellular accumulation of substrates. Mechanisms of lysosomal storage disorders include 1) primary deficiency of specific hydrolases; 2) defects in activator proteins required for enzyme-substrate interactions in posttranslational modification of enzymes or in transport of the substrate from lysosomes; and 3) abnormalities of fusion between autophagic vacuoles and lysosomes. Substrate accumulation is slowly progressive, leading to considerable morbidity and mortality.
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Cristina Vanrell, María, and Patricia Silvia Romano. "Close Encounters: Pathogenic Protists-Host Cell Interactions." In Phagocytosis - Main Key of Immune System [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.111398.

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In this chapter, we summarize the highlights of the early events in the interaction of parasitic protists and the host cell. Pathogenic protists are a group of eukaryotic organisms, responsible for causing different human diseases, such as malaria, Chagas disease, leishmaniasis, and toxoplasmosis. These pathogens display complex life cycles and go through different cellular transformations to adapt to the different hosts in which they live. Part of these life cycles takes place in mammals, inside the host cell. Host cell entry ends with the formation of phagosomes or parasitophorous vacuoles, which differ from each parasite and each type of host cell. While canonical phagocytosis involves the fusion of phagosomes with compartments of the endocytic pathway to produce normal maturation through the phagocytic route, pathogenic microorganisms have developed Different evasion mechanisms to resist the intracellular defense systems. These strategies, including phagosome maturation arrest, resistance to the harsh lysosomal environment, or exit to the host cell cytoplasm, will be also presented in this work.
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Tripathi, Anuj, and Smita Misra. "Vacuolar ATPase (V-ATPase) Proton Pump and Its Significance in Human Health." In Ion Transporters - From Basic Properties to Medical Treatment [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106848.

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Vacuolar H + -ATPases (V-ATPase), is an ATP-dependent proton transporter that transports protons across intracellular and cellular plasma membranes. V-ATPase is a multi-protein complex, which functions as an ATP-driven proton pump and is involved in maintaining pH homeostasis. The V-ATPase is a housekeeping proton pump and is highly conserved during evolution. The proton-pumping activity of V-ATPases allows acidification of intracellular compartments and influences a diverse range of cellular and biological processes. Thus, V-ATPase aberrant overexpression, mis-localization, and mutations in the genes for subunits are associated with several human diseases. This chapter focuses on a detailed view of V-type ATPase, and how V-ATPase contributes to human health and disease.
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M. Pike, Colleen, Rebecca R. Noll, and M. Ramona Neunuebel. "Exploitation of Phosphoinositides by the Intracellular Pathogen, Legionella pneumophila." In Pathogenic Bacteria. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89158.

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Manipulation of host phosphoinositide lipids has emerged as a key survival strategy utilized by pathogenic bacteria to establish and maintain a replication-permissive compartment within eukaryotic host cells. The human pathogen, Legionella pneumophila, infects and proliferates within the lung’s innate immune cells causing severe pneumonia termed Legionnaires’ disease. This pathogen has evolved strategies to manipulate specific host components to construct its intracellular niche termed the Legionella-containing vacuole (LCV). Paramount to LCV biogenesis and maintenance is the spatiotemporal regulation of phosphoinositides, important eukaryotic lipids involved in cell signaling and membrane trafficking. Through a specialized secretion system, L. pneumophila translocates multiple proteins that target phosphoinositides in order to escape endolysosomal degradation. By specifically binding phosphoinositides, these proteins can anchor to the cytosolic surface of the LCV or onto specific host membrane compartments, to ultimately stimulate or inhibit encounters with host organelles. Here, we describe the bacterial proteins involved in binding and/or altering host phosphoinositide dynamics to support intracellular survival of L. pneumophila.
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