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Academic literature on the topic 'Phagosome'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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Journal articles on the topic "Phagosome"

Lu, Nan, Qian Shen, Timothy R. Mahoney, Xianghua Liu, and Zheng Zhou. "Three sorting nexins drive the degradation of apoptotic cells in response to PtdIns(3)P signaling." Molecular Biology of the Cell 22, no. 3 (February 2011): 354–74. http://dx.doi.org/10.1091/mbc.e10-09-0756.

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Apoptotic cells are swiftly engulfed by phagocytes and degraded inside phagosomes. Phagosome maturation requires phosphatidylinositol 3-phosphate [PtdIns(3)P], yet how PtdIns(3)P triggers phagosome maturation remains largely unknown. Through a genome-wide PtdIns(3)P effector screen in the nematode Caenorhabditis elegans, we identified LST-4/SNX9, SNX-1, and SNX-6, three BAR domain-containing sorting nexins, that act in two parallel pathways to drive PtdIns(3)P-mediated degradation of apoptotic cells. We found that these proteins were enriched on phagosomal surfaces through association with PtdIns(3)P and through specific protein–protein interaction, and they promoted the fusion of early endosomes and lysosomes to phagosomes, events essential for phagosome maturation. Specifically, LST-4 interacts with DYN-1 (dynamin), an essential phagosome maturation initiator, to strengthen DYN-1’s association to phagosomal surfaces, and facilitates the maintenance of the RAB-7 GTPase on phagosomal surfaces. Furthermore, both LST-4 and SNX-1 promote the extension of phagosomal tubules to facilitate the docking and fusion of intracellular vesicles. Our findings identify the critical and differential functions of two groups of sorting nexins in phagosome maturation and reveal a signaling cascade initiated by phagocytic receptor CED-1, mediated by PtdIns(3)P, and executed through these sorting nexins to degrade apoptotic cells.

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Clemens, Daniel L., Bai-Yu Lee, and Marcus A. Horwitz. "Francisella tularensis Phagosomal Escape Does Not Require Acidification of the Phagosome." Infection and Immunity 77, no. 5 (February 23, 2009): 1757–73. http://dx.doi.org/10.1128/iai.01485-08.

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ABSTRACT Following uptake, Francisella tularensis enters a phagosome that acquires limited amounts of lysosome-associated membrane glycoproteins and does not acquire cathepsin D or markers of secondary lysosomes. With additional time after uptake, F. tularensis disrupts its phagosomal membrane and escapes into the cytoplasm. To assess the role of phagosome acidification in phagosome escape, we followed acidification using the vital stain LysoTracker red and acquisition of the proton vacuolar ATPase (vATPase) using immunofluorescence within the first 3 h after uptake of live or killed F. tularensis subsp. holarctica live vaccine strain (LVS) by human macrophages. Whereas 90% of the phagosomes containing killed LVS stained intensely for the vATPase and were acidified, only 20 to 30% of phagosomes containing live LVS stained intensely for the vATPase and were acidified. To determine whether transient acidification might be required for phagosome escape, we assessed the impact on phagosome permeabilization of the proton pump inhibitor bafilomycin A. Using electron microscopy and an adenylate cyclase reporter system, we found that bafilomycin A did not prevent phagosomal permeabilization by F. tularensis LVS or virulent type A strains (F. tularensis subsp. tularensis strain Schu S4 and a recent clinical isolate) or by “F. tularensis subsp. novicida,” indicating that F. tularensis disrupts its phagosomal membrane by a mechanism that does not require acidification.

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Sullivan, Jonathan Tabb, Ellen F. Young, Jessica R. McCann, and Miriam Braunstein. "The Mycobacterium tuberculosis SecA2 System Subverts Phagosome Maturation To Promote Growth in Macrophages." Infection and Immunity 80, no. 3 (January 3, 2012): 996–1006. http://dx.doi.org/10.1128/iai.05987-11.

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The ability ofMycobacterium tuberculosisto grow in macrophages is critical to the virulence of this important pathogen. One wayM. tuberculosisis thought to maintain a hospitable niche in macrophages is by arresting the normal process of phagosomes maturing into acidified phagolysosomes. The process of phagosome maturation arrest byM. tuberculosisis not fully understood, and there has remained a need to firmly establish a requirement for phagosome maturation arrest forM. tuberculosisgrowth in macrophages. Other intracellular pathogens that control the phagosomal environment use specialized protein export systems to deliver effectors of phagosome trafficking to the host cell. InM. tuberculosis, the accessory SecA2 system is a specialized protein export system that is required for intracellular growth in macrophages. In studying the importance of the SecA2 system in macrophages, we discovered that SecA2 is required for phagosome maturation arrest. Shortly after infection, phagosomes containing a ΔsecA2mutant ofM. tuberculosiswere more acidified and showed greater association with markers of late endosomes than phagosomes containing wild-typeM. tuberculosis. We further showed that inhibitors of phagosome acidification rescued the intracellular growth defect of the ΔsecA2mutant, which demonstrated that the phagosome maturation arrest defect of the ΔsecA2mutant is responsible for the intracellular growth defect. This study demonstrates the importance of phagosome maturation arrest forM. tuberculosisgrowth in macrophages, and it suggests there are effectors of phagosome maturation that are exported into the host environment by the accessory SecA2 system.

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Rupper, A. C., J. M. Rodriguez-Paris, B. D. Grove, and J. A. Cardelli. "p110-related PI 3-kinases regulate phagosome-phagosome fusion and phagosomal pH through a PKB/Akt dependent pathway in Dictyostelium." Journal of Cell Science 114, no. 7 (April 1, 2001): 1283–95. http://dx.doi.org/10.1242/jcs.114.7.1283.

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The Dictyostelium p110-related PI 3-kinases, PIK1 and PIK2, regulate the endosomal pathway and the actin cytoskeleton, but do not significantly regulate internalization of particles in D. discoideum. Bacteria internalized into (Δ)ddpik1/ddpik2 cells or cells treated with PI 3-kinase inhibitors remained intact as single particles in phagosomes with closely associated membranes after 2 hours of internalization, while in control cells, bacteria appeared degraded in multi-particle spacious phagosomes. Addition of LY294002 to control cells, after 60 minutes of chase, blocked formation of spacious phagosomes, suggesting PI 3-kinases acted late to regulate spacious phagosome formation. Phagosomes purified from control and drug treated cells contained equivalent levels of lysosomal proteins, including the proton pump complex, and were acidic, but in drug treated cells and (Δ)ddpik1/ddpik2 cells phagosomal pH was significantly more acidic during maturation than the pH of control phagosomes. Inhibition of phagosomal maturation by LY294002 was overcome by increasing phagosomal pH with NH(4)Cl, suggesting that an increase in pH might trigger homotypic phagosome fusion. A pkbA null cell line (PKB/Akt) reproduced the phenotype described for cells treated with PI 3-kinase inhibitors and (Δ)ddpik1/ddpik2 cells. We propose that PI 3-kinases, through a PKB/Akt dependent pathway, directly regulate homotypic fusion of single particle containing phagosomes to form multi-particle, spacious phagosomes, possibly through the regulation of phagosomal pH.

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Alvarez-Dominguez, C., R. Roberts, and P. D. Stahl. "Internalized Listeria monocytogenes modulates intracellular trafficking and delays maturation of the phagosome." Journal of Cell Science 110, no. 6 (March 15, 1997): 731–43. http://dx.doi.org/10.1242/jcs.110.6.731.

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Previous studies have shown that early phagosome-endosome fusion events following phagocytosis of Listeria monocytogenes are modulated by the live organism. In the present study, we have characterized more fully the intracellular pathway of dead and live Listeria phagosomes. To examine access of endosomal and lysosomal markers to phagosomes containing live and dead Listeria, quantitative electron microscopy was carried out with intact cells using internalized BSA-gold as a marker to quantify transfer of solute from endosomal and lysosomal compartments to phagosomes. To monitor the protein composition of phagosomal membranes and to quantify transfer of HRP from endosomes and lysosomes to phagosomes, highly enriched phagosomes containing live and dead Listeria were isolated. Enriched phagosomal membranes were used for western blotting experiments with endosomal and lysosomal markers. In this study, we used a listeriolysin-deficient mutant, Listeria(hly-), that is retained within the phagosome following phagocytosis. Western blotting experiments indicate that early endosomal markers (mannose receptor, transferrin receptor) and key fusion factors necessary for early events (NSF, alpha/beta-SNAP) but not late endosomal markers (cation dependent mannose 6-phosphate receptor) or lysosomal proteins (cathepsin D or lamp-1) accumulate on the live-Listeria phagosomal membranes. On the contrary, phagosomes containing dead-Listeria are readily accessible by both endocytic and lysosomal markers. Studies with radiolabeled dead- and live-Listeria(hly-) indicate that, following phagocytosis, degradation of the live microorganism is substantially delayed. These findings indicate that dead-Listeria containing phagosomes rapidly mature to a phagolysosomal stage whereas live-Listeria(hly-) prevents maturation, in part, by avoiding fusion with lysosomes. The data suggest that by delaying phagosome maturation and subsequent degradation, Listeria prolongs survival inside the phagosome/endosome assuring bacterial viability as a prelude to escape into the cytoplasm.

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Lerm, M., Å Holm, Å Seiron, E. Särndahl, K. E. Magnusson, and B. Rasmusson. "Leishmania donovani Requires Functional Cdc42 and Rac1 To Prevent Phagosomal Maturation." Infection and Immunity 74, no. 5 (May 2006): 2613–18. http://dx.doi.org/10.1128/iai.74.5.2613-2618.2006.

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ABSTRACT Leishmania donovani promastigotes survive inside macrophage phagosomes by inhibiting phagosomal maturation. The main surface glycoconjugate on promastigotes, lipophosphoglycan (LPG), is crucial for survival and mediates the formation of a protective shell of F-actin around the phagosome. Previous studies have demonstrated that this effect involves inhibition of protein kinase Cα. The present study shows that functional Cdc42 and Rac1 are required for the formation of F-actin around L. donovani phagosomes. Moreover, we present data showing that phagosomes containing LPG-defective L. donovani, which is unable to induce F-actin accumulation, display both elevated levels of periphagosomal F-actin and impaired phagosomal maturation in macrophages with permanently active forms of Cdc42 and Rac1. We conclude that L. donovani engages Cdc42 and Rac1 to build up a protective coat of F-actin around its phagosome to prevent phagosomal maturation.

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Garin, Jérome, Roberto Diez, Sylvie Kieffer, Jean-François Dermine, Sophie Duclos, Etienne Gagnon, Remy Sadoul, Christiane Rondeau, and Michel Desjardins. "The Phagosome Proteome." Journal of Cell Biology 152, no. 1 (January 8, 2001): 165–80. http://dx.doi.org/10.1083/jcb.152.1.165.

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Phagosomes are key organelles for the innate ability of macrophages to participate in tissue remodeling, clear apoptotic cells, and restrict the spread of intracellular pathogens. To understand the functions of phagosomes, we initiated the systematic identification of their proteins. Using a proteomic approach, we identified >140 proteins associated with latex bead–containing phagosomes. Among these were hydrolases, proton pump ATPase subunits, and proteins of the fusion machinery, validating our approach. A series of unexpected proteins not previously described along the endocytic/phagocytic pathways were also identified, including the apoptotic proteins galectin3, Alix, and TRAIL, the anti-apoptotic protein 14-3-3, the lipid raft-enriched flotillin-1, the anti-microbial molecule lactadherin, and the small GTPase rab14. In addition, 24 spots from which the peptide masses could not be matched to entries in any database potentially represent new phagosomal proteins. The elaboration of a two-dimensional gel database of >160 identified spots allowed us to analyze how phagosome composition is modulated during phagolysosome biogenesis. Remarkably, during this process, hydrolases are not delivered in bulk to phagosomes, but are instead acquired sequentially. The systematic characterization of phagosome proteins provided new insights into phagosome functions and the protein or groups of proteins involved in and regulating these functions.

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Lennon-Duménil, Ana-Maria, Arnold H. Bakker, René Maehr, Edda Fiebiger, Herman S. Overkleeft, Mario Rosemblatt, Hidde L. Ploegh, and Cécile Lagaudrière-Gesbert. "Analysis of Protease Activity in Live Antigen-presenting Cells Shows Regulation of the Phagosomal Proteolytic Contents During Dendritic Cell Activation." Journal of Experimental Medicine 196, no. 4 (August 19, 2002): 529–40. http://dx.doi.org/10.1084/jem.20020327.

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Here, we describe a new approach designed to monitor the proteolytic activity of maturing phagosomes in live antigen-presenting cells. We find that an ingested particle sequentially encounters distinct protease activities during phagosomal maturation. Incorporation of active proteases into the phagosome of the macrophage cell line J774 indicates that phagosome maturation involves progressive fusion with early and late endocytic compartments. In contrast, phagosome biogenesis in bone marrow–derived dendritic cells (DCs) and macrophages preferentially involves endocytic compartments enriched in cathepsin S. Kinetics of phagosomal maturation is faster in macrophages than in DCs. Furthermore, the delivery of active proteases to the phagosome is significantly reduced after the activation of DCs with lipopolysaccharide. This observation is in agreement with the notion that DCs prevent the premature destruction of antigenic determinants to optimize T cell activation. Phagosomal maturation is therefore a tightly regulated process that varies according to the type and differentiation stage of the phagocyte.

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VIEIRA, Otilia V., Roberto J. BOTELHO, and Sergio GRINSTEIN. "Phagosome maturation: aging gracefully." Biochemical Journal 366, no. 3 (September 15, 2002): 689–704. http://dx.doi.org/10.1042/bj20020691.

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Foreign particles and apoptotic bodies are eliminated from the body by phagocytic leucocytes. The initial stage of the elimination process is the internalization of the particles into a plasma membrane-derived vacuole known as the phagosome. Such nascent phagosomes, however, lack the ability to kill pathogens or to degrade the ingested targets. These properties are acquired during the course of phagosomal maturation, a complex sequence of reactions that result in drastic remodelling of the phagosomal membrane and contents. The determinants and consequences of the fusion and fission reactions that underlie phagosomal maturation are the topic of this review.

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Lee, Warren L., Moo-Kyung Kim, Alan D. Schreiber, and Sergio Grinstein. "Role of Ubiquitin and Proteasomes in Phagosome Maturation." Molecular Biology of the Cell 16, no. 4 (April 2005): 2077–90. http://dx.doi.org/10.1091/mbc.e04-06-0464.

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Phagosomes undergo multiple rounds of fusion with compartments of the endocytic pathway during the course of maturation. Despite the insertion of vast amounts of additional membrane, the phagosomal surface area remains approximately constant, implying active ongoing fission. To investigate the mechanisms underlying phagosomal fission we monitored the fate of Fcγ receptors (FcγR), which are known to be cleared from the phagosome during maturation. FcγR, which show a continuous distribution throughout the membrane of nascent phagosomes were found at later times to cluster into punctate, vesicular structures, before disappearing. In situ photoactivation of receptors tagged with a light-sensitive fluorescent protein revealed that some of these vesicles detach, whereas others remain associated with the phagosome. By fusing FcγR to pH-sensitive fluorescent proteins, we observed that the cytoplasmic domain of the receptors enters an acidic compartment, indicative of inward budding and formation of multivesicular structures. The topology of the receptor was confirmed by flow cytometry of purified phagosomes. Phagosomal proteins are ubiquitylated, and ubiquitylation was found to be required for formation of acidic multivesicular structures. Remarkably, proteasomal function is also involved in the vesiculation process. Preventing the generation of multivesicular structures did not impair the acquisition of late endosomal and lysosomal markers, indicating that phagosomal fusion and fission are controlled separately.

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Dissertations / Theses on the topic "Phagosome"

Guo, Manman. "Phagosome proteomes in activated macrophages." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/c5a94702-2164-4acc-9763-bdfcaf1229dc.

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Macrophages play key roles in innate and adaptive immune systems not only in the response to pathogens but also in tissue homeostasis. They are extremely plastic and recognize external stimuli such as cytokines with substantial changes to the proteome and molecular functions. One major macrophage function altered by cytokine activation is phagocytosis and phagosome maturation, through which macrophages engulf foreign material such as microbes or apoptotic cells to form phagosomes which then fuse with endosome and finally lysosomes, where the particles are finally degraded. My project aims at investigating the phagosome functions regulated in activated macrophages and further exploring the mechanism by which alternative activation regulates phagosome biogenesis. First of all, a comparison of phagosome proteomes of BMDMs and RAW 264.7 cells was performed, suggesting that there are significant differences for a large number of proteins including important receptors such as mannose receptor 1 and Siglec-1. Moreover, BMDM phagosomes mature considerably faster when validated using fluorogenic phagosome function assays. For the main goal of my project, I have performed a thorough proteomics analysis of the phagosome proteomes of non-activated (RestingMΦ), alternative-activated (IL4 treated, AAMΦ), classical-activated (LPS and IFNγ treated, CAMΦ) and reprogrammed (IL4 activated then LPS and IFNγ treated, ReMΦ) BMDMs. Results indicate that alternative activation leads to phagosomal recruitment of proteins in favour of apoptotic cell clearance, enhanced fusion with lysosomes as well as with parts of the endoplasmic reticulum (ER). Both proteomics and phagosome function assays showed that the phagosome maturation is enhanced in AAMΦ and reduced in CAMΦ and ReMΦ. As side projects, I have also compared phagosome proteomes in IL4 treated, IL13 treated and IL10 treated BMDMs and analysed cellular total proteomes of AAMΦ and RestingMΦ. Furthermore, proteomic data suggest the specific recruitment of TAK1/MKK7/JNK signalling to the phagosomes in AAMΦ, which was confirmed by immunoblotting and fluorescence microscopy. I uncovered that K63 polyubiquitylation of phagosomal proteins is enhanced in AAMΦ, which is responsible for the translocation of TAK1 complex. In AAMΦ, 55 K63 polyubiquitylation sites on 33 phagosomal proteins were identified, including macrophage scavenger receptor 1 (MSR1/SRA). This receptor was further found to be specifically polyubiquitylated on phagosomes upon alternative activation, and MSR1 activation leads to enhanced JNK activation in AAMΦ. Finally, three hypotheses of the function of JNK pathway on phagosomes were described. Firstly, proteomics reveals a reduction of ER and lipid metabolic proteins to phagosomes by the inhibition of JNK, suggesting that TAK1/MKK7/JNK signalling might regulate phagosomal lipid handling. Secondly, JNK might phosphorylate the lipid-activated transcription factor, PPARγ, to regulate macrophage gene expression in lipid metabolism. Finally, loss of MSR1 impairs oxLDL induced JNK activation and M2-to-M1 shift of macrophages, indicating that MSR1/JNK cascade mediates phenotypic shift of AAMΦ upon lipid laden. In conclusion, the work in this thesis provides comprehensive characterisation of phagosomal and cellular proteomes in activated BMDMs. Moreover, TAK1/MKK7/JNK signalling was found for the first time to be specially recruited to phagosomes by K63 polyubiquitylation, and 55 novel K63 polyubiquitylation sites on 33 phagosomal proteins were identified, including MSR1. We hypothesise that JNK signalling might regulate lipid metabolism in AAMΦ.

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Smith, Leanne May. "Investigating phagosome dynamics of microbial pathogens." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/4937/.

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Many microbial pathogens are able to evade killing by phagocytes of the innate immune system. This thesis focuses on two pathogens: the fungal pathogen \(Cryptococcus\) \(neoformans\) and the bacterial pathogen \(Streptococcus\) \(agalactiae\). \(C\). \(neoformans\) causes severe cryptococcal meningitis in mostly immunocompromised hosts, such as those with HIV infection. In contrast, \(S\). \(agalactiae\) is the leading cause of neonatal sepsis and meningitis. The interaction between macrophages and these pathogens is likely to be critical in determining dissemination and outcome of disease in both instances. A collection of \(S\). \(agalactiae\) clinical isolates, ranging in origin from colonisation cases to severe infection cases, were tested for their ability to persist with a macrophage cell line. Surprisingly, persistence within macrophages was a characteristic shared by all of the isolates tested. Furthermore, by investigating the \(Streptococcus\)-containing phagosome, it was revealed that streptococci are able to manipulate the acidification of macrophage phagosomes. Similarly, the maturation of phagosomes containing the fungal pathogen \(C\). \(neoformans\) was explored. Cryptococci are shown to be able to manipulate the phagosome they reside within. This is driven by modified acquisition of Rab GTPases to the phagosome, as well as altered acidification and cathepsin activity within \(Cryptococcus\)-containing phagosomes.

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Boucherit, Nicolas. "Mécanisme d'interférence de la conversion du phagosome par Coxiella burnetii." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5061/document.

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Pour survivre et se multiplier dans leurs cellules hôtes les bactéries intracellulaires ont élaboré divers mécanismes d'échappement à la réponse immunitaire. L’altération du trafic intracellulaire est une des stratégies utilisée par ces agents pathogènes. Ainsi Coxiella burnetii, bactérie intracellulaire stricte responsable chez l’homme de la fièvre Q, bloque la maturation du phagosome afin de résider et se multiplier dans un compartiment incapable de fusionner avec les lysosomes. Ce défaut de fusion est associé à la virulence bactérienne. Pour analyser le défaut de maturation du phagosome de C. burnetii, j’ai étudié le rôle du lipopolysaccharide (LPS) de C. burnetii dans le trafic intracellulaire de cette bactérie. J’ai montré que le LPS de C. burneti, unique par sa structure, ne permet pas l’activation de la MAPKinase p38α, entrainant un défaut dans le recrutement du complexe HOPS (homotypic fusion and vacuole protein sorting complex) nécessaire à la conversion phagosomale. J’ai en effet montré que le recrutement du complexe HOPS requiert la phosphorylation de la protéine Vps (vacuolar protein sorting) 41. La transfection de macrophages permettant la surexpression d’un activateur de p38 et l’utilisation de mutants phosphomimétiques de Vps41 ont montré une restauration de la conversion phagosomale. Il apparaît ainsi que la MAPK-p38α et son dialogue avec Vps41 jouent un rôle central dans la maturation du phagosome de C. burnetii en phagolysosome. L’utilisation de la structure atypique de son LPS permet ainsi à C. burnetii de se soustraire à la réponse protectrice de l'hôte
To survive and replicate in their host, microbes have evolved several strategies to hijack the microbicidal properties of the immune cells. C. burnetii, the q fever agent, survive and replicate in macrophages through the alteration of the phago-lysosome biogenesis. To further analyze the nature of the defect phagosome maturation of C. burnetii, I studied the role of lipopolysaccharide (LPS) of C. burnetii in the intracellular trafficking of the bacteria. The LPS is unable to activate the p38α MAPKinase, which explains that the virulent bacteria are not directed to a degradative compartment . The lack of activation of the p38α MAPKinase , which involves a commitment TLR4 antagonist by LPS, has the effect of preventing the recruitment of the HOPS complex ( homotypic fusion and vacuole protein sorting complex) , a complex require for the phagosomal conversion. I have shown that the recruitment of HOPS requires phosphorylation of protein Vps (vacuolar protein sorting) 41. Transfection of macrophages by an activator of p38 and using phosphomimétiques mutants VPS41 showed restoration of phagosome maturation. It thus appears that the p38α MAPK and his dialogue with VPS41 play a central role in phagosome maturation of C. burnetii in the phagolysosome. Use of the unique structure of the LPS allows C. burnetii to evade the protective response of the host

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Pietersen, Ray-Dean Donovan. "Proteomic analysis of the Mycobacterium avium-containing phagosome membrane." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/12226.

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Includes bibliographical references (leaves 139-158).
Pathogenic mycobacteria, like [Mycobacterium tuberculosis] M.tb and Mycobacterium avium (M.av), reside intracellularly in phagosomes where they are able to survive, because they block the process of phagosome maturation. ... An approach of characterizing M.av-containing phagosomes in terms of cell surface-derived glycoconjugates, revealed that these phagosomes show a 3- to 4-fold depletion of these glycoconjugates as compared to early endosomes with which the phagosomes continuously fuse and exchange membrane molecules... The aim of this study is to identify the depleted / possibly enriched cell surface derived glycoproteins on the phagosome membrane of M.av-containing phagosomes, because they might play a role in mycobacteria's intracellular survival.

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Geffken, Anna Christina [Verfasser]. "Mycobacterium tuberculosis – host-cell interactions in the phagosome / Anna Christina Geffken." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2016. http://d-nb.info/1098170482/34.

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Hackam, David Joel. "Mechanisms of phagosome formation, maturation and acidification, implications for intracellular infection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0003/NQ41434.pdf.

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Bajno, Lydia. "Focal exocytosis of VAMP3-containing vesicles at sites of phagosome formation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ53328.pdf.

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Schnettger, L. "The role of the small GTPase Rab20 in Mycobacterium tuberculosis phagosome biology." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1532039/.

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Mycobacterium tuberculosis is an intracellular pathogen that arrests phagosome maturation to survive within macrophages and cause disease. The process of phagosome maturation is important for the innate immunity against intracellular pathogens as well as the adaptive immunity and antigen processing. Activation by cytokines such as IFN-γ can modulate immune responses to infection. Several Rab GTPases regulate M. tuberculosis phagosome maturation, highlighting the importance of intracellular trafficking in this process. There is compelling evidence that M. tuberculosis can colonise several niches within macrophages, both in heterogeneous membrane-bound compartments as well as in the cytosol. In this thesis, the control of M. tuberculosis infection by IFN-γ through modulation of intracellular trafficking and thereby the intracellular niche occupied by this pathogen was investigated. First, a novel IFN-γ/Rab20 dependent pathway that targets pathogens into spacious phagosomes for elimination in macrophages is described. IFN-γ induced Rab20 expression and association with phagosomes. The analysis of spatiotemporal dynamics of M. tuberculosis phagosomes showed that in contrast to Rab5, PI3P or Rab7; EGFP-Rab20 was retained on M. tuberculosis phagosomes for up to 24 hours, which was comparable to endogenous Rab20 association with M. tuberculosis phagosomes in IFN-γ activated macrophages. IFN-γ increased interaction of M. tuberculosis phagosomes with the endosomal network via Rab20, targeting mycobacteria to spacious, proteolytic compartments resulting in inhibition of M. tuberculosis growth. Furthermore, this targeting of M. tuberculosis to spacious phagosomes reduced phagosomal damage and access of mycobacteria to the cytosol. In resting macrophages, M. tuberculosis was able to subvert this targeting to spacious compartments in a manner that was dependent on its ESX-1 secretion system. Altogether, this work reports a cell-autonomous, IFN-γ/Rab20 dependent pathway that results in elimination of M. tuberculosis by retention of mycobacteria in membrane-bound spacious compartments.

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Pei, Gang [Verfasser], and Michael [Akademischer Betreuer] Steinert. "Role of Rab20 in phagosome maturation and mycobacterial killing / Gang Pei ; Betreuer: Michael Steinert." Braunschweig : Technische Universität Braunschweig, 2013. http://d-nb.info/1175822019/34.

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Bilkei-Gorzo, Orsolya. "Ubiquitylation regulates vesicle trafficking and innate immune responses on the phagosome of inflammatory macrophages." Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/8661922d-9d5e-4a4a-bfd4-b0f5e5717c61.

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Macrophages are sentinels present in most tissues of the body, where they recognise and respond to biological dangers. Recognition and uptake of particles is mediated through phagocytic receptors which upon activation induce appropriate responses. These responses need to be tightly regulated in order to destroy pathogens but prevent uncontrolled inflammation. Phagocytosis is an evolutionarily conserved process required for host defence and homeostasis. During phagocytosis, particles are recognised by cell surface receptors that trigger rearrangement of the actin cytoskeleton and internalization of the bound particle into a de novo, membranous organelle known as the phagosome. Regulation of phagocytosis and phagosome maturation can be achieved through changes in transcription/translation and differential recruitment of proteins but also through their non-translational modifications. Here I explored the role of ubiquitylation in the phagosome biogenesis of Interferon-gamma (IFN-ɣ) activated macrophages. Ubiquitylation is a diverse, reversible post-translational modification which is not only involved in protein degradation but also in vesicle trafficking and immune signalling. My data shows that phagosomes are enriched in polyubiquitylation, which is further enhanced by IFN-ɣ. I applied a targeted AQUA peptide approach by which we quantified ubiquitin chain linkage peptides from phagosome samples by PRM. This data shows that all chain linkages apart from M1/linear chains are present on phagosomes. Furthermore, IFN-ɣ activation enhanced K11, K48 and K63 chains significantly. In order to identify the molecular function of this polyubiquitylation, I characterized the ubiquitinome of phagosomes of IFN-γ activated macrophages and can demonstrate that ubiquitylation is preferentially attached to proteins involved in vesicle trafficking, thereby delaying fusion with late endosomes and lysosomes. I demonstrated that most ubiquitin chains are on the cytoplasmic site of the phagosome enabling an interaction of ubiquitin chains with cytosolic proteins such as Rab7. Rab7 a major regulator of vesicle trafficking could be shown to be ubiquitylated on phagosomes. I further showed that phagosomal recruitment of the E3 ligase RNF115 is enhanced upon IFN-γ stimulation and RNF115 is responsible for most of the increase of K63 polyubiquitylation of phagosomal proteins. Knock-down of RNF115 promotes phagosome maturation and induces an increased pro-inflammatory response to Toll-like receptor (TLR) agonists, indicating that RNF115 is a negative regulator of vesicular trafficking to the lysosome and disruption of this pathway induces pro-inflammatory responses in macrophages. In conclusion, this is the first study showing unbiasedly that ubiquitylation plays an important role in vesicle trafficking to the lysosome.

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Books on the topic "Phagosome"

Deretic, Vojo, ed. Autophagosome and Phagosome. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4.

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Bajno, Lydia. Focal exocytosis of VAMP3-containing vesicles at sites of phagosome formation. Ottawa: National Library of Canada, 2000.

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Botelho, Roberto, ed. Phagocytosis and Phagosomes. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6581-6.

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Vojo, Deretic, ed. Autophagosome and phagosome / edited by Vojo Deretic. Totowa, NJ: Humana Press, 2008.

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Scott, Cameron. Control of phagocytosis and phagosome maturation by phosphoinositides. 2005.

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Lee, Warren Lester. Membrane remodelling and signal transduction during phagosome formation and maturation. 2006.

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Hackam, David Joel. Mechanisms of phagosome formation, maturation and acidification: Implications for intracellular infection. 1998.

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Tan, Tracy. The ESAT-6/CFP-10 secretion system of Mycobacterium marinum modulates phagosome maturation. 2006.

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Paroutis, Paul. Quantitative and dynamic assessment of the contribution of the endoplasmic reticulum to phagosome formation. 2005.

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Botelho, Roberto J. Lipid signaling and the role of COPI in Fc[gamma] receptor-mediated phagocytosis and phagosome maturation. 2004.

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Book chapters on the topic "Phagosome"

Gooch, Jan W. "Phagosome." In Encyclopedic Dictionary of Polymers, 914. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14473.

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Deretic, Vojo. "Autophagosome and Phagosome." In Autophagosome and Phagosome, 1–10. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_1.

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Young, Andrew, and Sharon Tooze. "Protein Trafficking into Autophagosomes." In Autophagosome and Phagosome, 147–57. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_10.

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Lavieu, Grégory, Francesca Scarlatti, Giusy Sala, Stéphane Carpentier, Thierry Levade, Riccardo Ghidoni, Joëlle Botti, and Patrice Codogno. "Sphingolipids in Macroautophagy." In Autophagosome and Phagosome, 159–73. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_11.

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Ciechomska, Iwona A., Christoph G. Goemans, and Aviva M. Tolkovsky. "Molecular Links Between Autophagy and Apoptosis." In Autophagosome and Phagosome, 175–93. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_12.

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Ravikumar, Brinda, Sovan Sarkar, and David C. Rubinsztein. "Clearance of Mutant Aggregate-Prone Proteins by Autophagy." In Autophagosome and Phagosome, 195–211. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_13.

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Schmid, Dorothee, and Christian Münz. "Localization and MHC Class II Presentation of Antigens Targeted for Macroautophagy." In Autophagosome and Phagosome, 213–25. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_14.

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Kaushik, S., and A. M. Cuervo. "Chaperone-Mediated Autophagy." In Autophagosome and Phagosome, 227–44. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_15.

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Uttenweiler, Andreas, and Andreas Mayer. "Microautophagy in the Yeast Saccharomyces cerevisiae." In Autophagosome and Phagosome, 245–59. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_16.

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Chastellier, Chantal. "EM Analysis of Phagosomes." In Autophagosome and Phagosome, 261–85. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-157-4_17.

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Conference papers on the topic "Phagosome"

Crouser, E. D., L. W. Locke, M. W. Julian, S. Bicer, P. White, and L. S. Schlesinger. "Phagosome-Regulated-mTOR Signaling During Sarcoidosis Granulomagenesis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3102.

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Cheng, Wenhao, Sundol Kim, Sandra Zivkovic, Yi Ren, Hoyong Chung, and Jingjiao Guan. "Tracking Phagosome-Derived Vesicles in Macrophages with Microfabricated Microparticles." In The 6th World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2021. http://dx.doi.org/10.11159/nddte21.lx.203.

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Daniel, Rebekah, Andrew T. Koll, and David Altman. "Force dependence of phagosome trafficking in retinal pigment epithelial cells." In SPIE NanoScience + Engineering, edited by Kishan Dholakia and Gabriel C. Spalding. SPIE, 2014. http://dx.doi.org/10.1117/12.2062055.

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O'Leary, SM, M. O'Sullivan, DM Kelly, R. Ryan, and J. Keane. "IL-10 Blocks Phagosome Maturation in Human Macrophages Infected with M. tuberculosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5103.

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Alhousseiny, Sara. "The role of the autophagy pathway in phagosome formation in macrophages interacting with adipocytes." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2018. http://dx.doi.org/10.5339/qfarc.2018.hbpd154.

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Oberley-Deegan, RE, Y. Lee, GE Morey, DM Cook, ED Chan, and JD Crapo. "MnTE-2-PyP, an Antioxidant Mimetic, Reduces Intracellular Growth ofMycobacterium abscessusby Enhancing Phagosome-Lysosome Fusion." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5104.

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Jubrail, Jamil, Kshanti Africano-Gomez, Floriane Herit, Pierre-Regis Burgel, Lisa Oberg, Elisabeth Israelsson, Kristofer Thorn, et al. "Human rhinovirus 16 infection of human macrophages impairs their clearance ability by perturbing phagosome maturation." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4977.

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van Ingen, Jakko, Diane Houben, Nicole N. van der Wel, Richard Dekhuijzen, Martin J. Boeree, and Dick van Soolingen. "The Clinical Relevance Of Mycobacterium Szulgai And M. Kansasii Type I Is Explained By Translocation From The Phagosome To The Cytosol Of Human Macrophages." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2610.

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Yoon, Jonghee, Kyoohyun Kim, Jaehwang Jung, and YongKeun Park. "3-D quantitative tracking of phagosomes using quantitative phase microscopy." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2014. http://dx.doi.org/10.1364/acpc.2014.ath1d.5.

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Ufimtseva, Elena, Natalya Eremeeva, Diana Vakhrusheva, and Sergey Skornyakov. "Mycobacterium tuberculosis reside only inside phagosomes in alveolar macrophages of tuberculosis patients." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4730.

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