Готові списки джерел за темами / LC3 associated phagocytosis (LAP)

Добірка наукової літератури з теми "LC3 associated phagocytosis (LAP)"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "LC3 associated phagocytosis (LAP)"

Yuan, Jin, Qiuyu Zhang, Shihua Chen, Min Yan, and Lei Yue. "LC3-Associated Phagocytosis in Bacterial Infection." Pathogens 11, no. 8 (July 30, 2022): 863. http://dx.doi.org/10.3390/pathogens11080863.

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LC3-associated phagocytosis (LAP) is a noncanonical autophagy process reported in recent years and is one of the effective mechanisms of host defense against bacterial infection. During LAP, bacteria are recognized by pattern recognition receptors (PRRs), enter the body, and then recruit LC3 onto a single-membrane phagosome to form a LAPosome. LC3 conjugation can promote the fusion of the LAPosomes with lysosomes, resulting in their maturation into phagolysosomes, which can effectively kill the identified pathogens. However, to survive in host cells, bacteria have also evolved strategies to evade killing by LAP. In this review, we summarized the mechanism of LAP in resistance to bacterial infection and the ways in which bacteria escape LAP. We aim to provide new clues for developing novel therapeutic strategies for bacterial infectious diseases.

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Duan, Zhimin, Qing Chen, Leilei Du, Jianbo Tong, Song Xu, Rong Zeng, Yuting Ma, Xu Chen, and Min Li. "Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/4938649.

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Autophagy machinery has roles in the defense against microorganisms such as Candida albicans. Lipidated LC3, the marker protein of autophagy, participates in the elimination of C. albicans by forming a single-membrane phagosome; this process is called LC3-associated phagocytosis (LAP). However, the influence of C. albicans on autophagic flux is not clear. In this study, we found that C. albicans inhibited LC3 turnover in macrophages. After the phagocytosis of C. albicans in macrophages, we observed fewer acridine orange-positive vacuoles and RFP-GFP-LC3 puncta without colocalization with phagocytized C. albicans. However, phagocytosis of C. albicans led to LC3 recruitment, but p62 and ATG9A did not colocalize with LC3 or C. albicans. These effects are due to an MTOR-independent pathway. Nevertheless, we found that the C. albicans pattern-associated molecular pattern β-glucan increased LC3 turnover. In addition, phagocytosis of C. albicans caused a decrease in BrdU incorporation. Blocking autophagic flux aggravated this effect. Our findings suggest that phagocytosis of C. albicans decreases autophagic flux but induces LAP in an MTOR-independent manner in macrophages. Occupation of LC3 by recruiting engulfed C. albicans might contribute to the inhibition of autophagic flux. Our study highlights the coordinated machinery between canonical autophagy and LAP that defends against C. albicans challenge.

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Galais, Mathilde, Baptiste Pradel, Isabelle Vergne, Véronique Robert-Hebmann, Lucile Espert, and Martine Biard-Piechaczyk. "La phagocytose associée à LC3 (LAP)." médecine/sciences 35, no. 8-9 (August 2019): 635–42. http://dx.doi.org/10.1051/medsci/2019129.

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Phagocytose et macroautophagie, appelée ici autophagie, sont deux mécanismes essentiels de dégradation lysosomale de divers cargos englobés dans des structures membranaires. Ils sont tous deux impliqués dans la régulation du système immunitaire et la survie cellulaire. Cependant, la phagocytose permet l’ingestion de matériel extracellulaire alors que l’autophagie dégrade des composants intra-cytoplasmiques, avec des mécanismes d’activation et de maturation différents. La LAP (LC3-associated phagocytosis) est une forme particulière de phagocytose qui utilise certains éléments de l’autophagie. Elle permet l’élimination de pathogènes, de complexes immuns, de cellules avoisinantes, mortes ou vivantes, constituant un danger pour l’organisme, et de débris cellulaires, tels que les segments externes des photorécepteurs (POS, photoreceptor outer segment), ou la pièce centrale du pont intercellulaire produit en fin de mitose. Les cellules ont ainsi « optimisé » leurs moyens d’éliminer les composés potentiellement dangereux en partageant certains éléments essentiels des deux voies de dégradation lysosomale.

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Lai, Shu-chin, and Rodney J. Devenish. "LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy." Cells 1, no. 3 (July 30, 2012): 396–408. http://dx.doi.org/10.3390/cells1030396.

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Morita, Maya, Mayu Kajiye, Chiye Sakurai, Shuichi Kubo, Miki Takahashi, Daiki Kinoshita, Naohiro Hori, and Kiyotaka Hatsuzawa. "Characterization of MORN2 stability and regulatory function in LC3-associated phagocytosis in macrophages." Biology Open 9, no. 6 (May 15, 2020): bio051029. http://dx.doi.org/10.1242/bio.051029.

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ABSTRACTMicrotubule-associated protein A1/B1-light chain 3 (LC3)-associated phagocytosis (LAP) is a type of non-canonical autophagy that regulates phagosome maturation in macrophages. However, the role and regulatory mechanism of LAP remain largely unknown. Recently, the membrane occupation and recognition nexus repeat-containing-2 (MORN2) was identified as a key component of LAP for the efficient formation of LC3-recruiting phagosomes. To characterize MORN2 and elucidate its function in LAP, we established a MORN2-overexpressing macrophage line. At a steady state, MORN2 was partially cleaved by the ubiquitin-proteasome system. MORN2 overexpression promoted not only LC3-II production but also LAP phagosome (LAPosome) acidification during Escherichia coli uptake. Furthermore, the formation of LAPosomes containing the yeast cell wall component zymosan was enhanced in MORN2-overexpressing cells and depended on reactive oxygen species (ROS). Finally, MORN2-mediated LAP was regulated by plasma membrane-localized soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) such as SNAP-23 and syntaxin 11. Taken together, these findings demonstrate that MORN2, whose expression is downregulated via proteasomal digestion, is a limiting factor for LAP, and that membrane trafficking by SNARE proteins is involved in MORN2-mediated LAP.

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Martinez, Jennifer, Andrew Oberst, Thirumala Devi-Kanneganti, and Douglas Green. "LC3-associated phagocytosis is a critical regulator of innate immunity. (P1261)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 56.13. http://dx.doi.org/10.4049/jimmunol.190.supp.56.13.

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Abstract The magnitude and quality of the innate immune response is shaped by many factors, both cell-intrinsic and -extrinsic. The process of autophagy is a cell-intrinsic pathway that has been implicated in the suppression of innate pro-inflammatory cytokines, and polymorphisms in autophagy genes (ATG16L) have been linked to inflammatory disease. A similar but distinct pathway, LC3-associated phagocytosis (LAP), is also important in shaping innate immune responses, largely by linking the sensing of PAMPS to the autophagic machinery, a process critical for the clearance of both pathogens and dead host cells. As autoimmunity may arise from a failure to engulf or degrade dying cells, we sought to determine if LAP might function to dampen inflammatory responses by halting otherwise constitutive signals from within the phagosome. Indeed, we show that mice with phagocytes deficient for LAP machinery (such as ATG7) exhibit increased pro-inflammatory cytokines levels in the serum when challenged with exogenous dead cells. Moreover, successful clearance of the pathogen Listeria monocytogenes requires LAP, rather than conventional autophagy. In order to fully understand this distinct and vital mechanism for effective host defense, it will be necessary to identify molecular events that are unique to LAP, which will allow us to further distinguish the physiological and pathological roles for LAP.

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Wen, Haitao, Tianliang Li, Xinghui Li, Yu Lei, and Douglas R. Green. "Mitochondrial Calcium Signaling Facilitates Bacterial Survival by Restraining LC3-associated Phagocytosis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 227.1. http://dx.doi.org/10.4049/jimmunol.204.supp.227.1.

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Abstract Mitochondria in eukaryotic cells are believed to have originated from proteobacteria through endosymbiosis 2.5 billion years ago. Accumulating evidence suggests essential roles of mitochondria in host defense response against invading pathogens. Whether intracellular bacteria can hijack mitochondria to promote their survival remains elusive. Here, we demonstrate a previously unappreciated pro-survival strategy employed by intracellular bacteria Listeria monocytogenesthat involves the suppression of LC3-associated phagocytosis (LAP) by mitochondrial Ca2+ signaling. Invasion of macrophages by L. monocytogenes caused a robust mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), leading to elevated acetyl-coenzyme A (acetyl-CoA) production via the pyruvate dehydrogenase (PDH). Acetylation of LAP effector Rubicon with the use of acetyl-CoA antagonized LAP formation. Genetic ablation of Mcuimproved bacterial killing due to elevated LAP formation. Our study indicates that modulation of mitochondrial Ca2+ signaling is a beneficial strategy for bacterial survival and highlights the importance of mitochondrial metabolism in host-microbial interaction.

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Inomata, Megumi, Shuying Xu, Pallavi Chandra, Simin N. Meydani, Genzou Takemura, Jennifer A. Philips, and John M. Leong. "Macrophage LC3-associated phagocytosis is an immune defense against Streptococcus pneumoniae that diminishes with host aging." Proceedings of the National Academy of Sciences 117, no. 52 (December 21, 2020): 33561–69. http://dx.doi.org/10.1073/pnas.2015368117.

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Streptococcus pneumoniae is a leading cause of pneumonia and invasive disease, particularly, in the elderly. S. pneumoniae lung infection of aged mice is associated with high bacterial burdens and detrimental inflammatory responses. Macrophages can clear microorganisms and modulate inflammation through two distinct lysosomal trafficking pathways that involve 1A/1B-light chain 3 (LC3)-marked organelles, canonical autophagy, and LC3-associated phagocytosis (LAP). The S. pneumoniae pore-forming toxin pneumolysin (PLY) triggers an autophagic response in nonphagocytic cells, but the role of LAP in macrophage defense against S. pneumoniae or in age-related susceptibility to infection is unexplored. We found that infection of murine bone-marrow-derived macrophages (BMDMs) by PLY-producing S. pneumoniae triggered Atg5- and Atg7-dependent recruitment of LC3 to S. pneumoniae-containing vesicles. The association of LC3 with S. pneumoniae-containing phagosomes required components specific for LAP, such as Rubicon and the NADPH oxidase, but not factors, such as Ulk1, FIP200, or Atg14, required specifically for canonical autophagy. In addition, S. pneumoniae was sequestered within single-membrane compartments indicative of LAP. Importantly, compared to BMDMs from young (2-mo-old) mice, BMDMs from aged (20- to 22-mo-old) mice infected with S. pneumoniae were not only deficient in LAP and bacterial killing, but also produced higher levels of proinflammatory cytokines. Inhibition of LAP enhanced S. pneumoniae survival and cytokine responses in BMDMs from young but not aged mice. Thus, LAP is an important innate immune defense employed by BMDMs to control S. pneumoniae infection and concomitant inflammation, one that diminishes with age and may contribute to age-related susceptibility to this important pathogen.

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Wan, JingHong, Emmanuel Weiss, Sanae Ben Mkaddem, Morgane Mabire, Pierre-Marie Choinier, Olivia Picq, Tristan Thibault-Sogorb, et al. "LC3-associated phagocytosis protects against inflammation and liver fibrosis via immunoreceptor inhibitory signaling." Science Translational Medicine 12, no. 539 (April 15, 2020): eaaw8523. http://dx.doi.org/10.1126/scitranslmed.aaw8523.

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Sustained hepatic and systemic inflammation, particularly originating from monocytes/macrophages, is a driving force for fibrosis progression to end-stage cirrhosis and underlies the development of multiorgan failure. Reprogramming monocyte/macrophage phenotype has emerged as a strategy to limit inflammation during chronic liver injury. Here, we report that LC3-associated phagocytosis (LAP), a noncanonical form of autophagy, protects against hepatic and systemic inflammation during chronic liver injury in rodents, with beneficial antifibrogenic effects. LAP is enhanced in blood and liver monocytes from patients with fibrosis and cirrhosis. Pharmacological inhibition of LAP components in human monocytes from patients with cirrhosis or genetic disruption of LAP in mice with chronic liver injury exacerbates both the inflammatory signature in isolated human monocytes and the hepatic inflammatory profile in mice, resulting in enhanced liver fibrosis. Mechanistically, patients with cirrhosis showed increased monocyte expression of Fc fragment of IgG receptor IIA (FcγRIIA) and enhanced engulfment of immunoglobulin G in LC3+ phagosomes that triggers an FcγRIIA/Src homology region 2 domain–containing phosphatase-1 (SHP-1) inhibitory immunoreceptor tyrosine-based activation motif (ITAMi) anti-inflammatory pathway. Mice overexpressing human FcγRIIA in myeloid cells show enhanced LAP in response to chronic liver injury and resistance to inflammation and liver fibrosis. Activation of LAP is lost in monocytes from patients with multiorgan failure and restored by specifically targeting ITAMi signaling with anti-FcγRIIA F(ab′)2 fragments, or with intravenous immunoglobulin (IVIg). These data suggest the existence of an ITAMi-mediated mechanism by which LAP might protect against inflammation. Sustaining LAP may open therapeutic perspectives for patients with chronic liver disease.

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Li, Xuelei, Mark Prescott, Ben Adler, John D. Boyce, and Rodney J. Devenish. "Beclin 1 Is Required for Starvation-Enhanced, but Not Rapamycin-Enhanced, LC3-Associated Phagocytosis of Burkholderia pseudomallei in RAW 264.7 Cells." Infection and Immunity 81, no. 1 (October 31, 2012): 271–77. http://dx.doi.org/10.1128/iai.00834-12.

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LC3-associated phagocytosis (LAP) ofBurkholderia pseudomalleiby murine macrophage (RAW 264.7) cells is an intracellular innate defense mechanism. Beclin 1, a protein with several roles in autophagic processes, is known to be recruited to phagosomal membranes as a very early event in LAP. We sought to determine whether knockdown of Beclin 1 by small interfering RNA (siRNA) would affect recruitment of LC3 and subsequent LAP of infectingB. pseudomallei. Both starvation and rapamycin treatment can induce Beclin 1-dependent autophagy. Therefore, we analyzed the consequences of Beclin 1 knockdown for LAP in infected cells that had been either starved or treated with rapamycin by determining the levels of bacterial colocalization with LC3 and intracellular survival. Concurrently, we confirmed the location of bacteria as either contained in phagosomes or free in the cytoplasm. We found that both rapamycin and starvation treatment enhanced LAP ofB. pseudomalleibut that the rapamycin response is Beclin 1 independent whereas the starvation response is Beclin 1 dependent.

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Більше джерел

Дисертації з теми "LC3 associated phagocytosis (LAP)"

Gluschko, Alexander [Verfasser], and Thorsten [Gutachter] Hoppe. "LC3-associated Phagocytosis induced by the ß2 integrin Mac-1 enhances Immunity to Infection with Listeria monocytogenes / Alexander Gluschko ; Gutachter: Thorsten Hoppe." Köln : Universitäts- und Stadtbibliothek Köln, 2018. http://d-nb.info/1165772752/34.

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Stetter, Maurice [Verfasser], Antje [Gutachter] Gohla, Wolfgang [Gutachter] Kastenmüller, and Ann [Gutachter] Wehman. "LC3-associated phagocytosis seals the fate of the second polar body in \(Caenorhabditis\) \(elegans\) / Maurice Stetter ; Gutachter: Antje Gohla, Wolfgang Kastenmüller, Ann Wehman." Würzburg : Universität Würzburg, 2021. http://d-nb.info/123075864X/34.

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Ligeon, Laure-Anne. "Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie." Thesis, Lille 2, 2013. http://www.theses.fr/2013LIL2S043/document.

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Yersinia pseudotuberculosis appartient à la famille des Enterobacteriaceae et peut être responsable de syndromes articulaires et digestifs. Au cours de la colonisation de l’hôte, une minorité des bactéries va, en plus de l’étape de multiplication extracellulaire présenter une phase de réplication intracellulaire dans les macrophages. Une partie des Y. pseudotuberculosis va se répliquer dans les macrophages en usurpant la voie de l’autophagie, afin de créer une niche réplicative au sein des autophagosomes bloqués dans leur maturation. Le trafic membranaire associé à l’infection de Y. pseudotuberculosis reste à ce jour peu caractérisé. Dans un premier temps, nous avons observé que lors de l’infection d’une cellule épithéliale par Y. pseudotuberculosis, la vacuole bactérienne est associée avec le marqueur des autophagosomes, la protéine LC3 mais de façon surprenante cette vacuole ne présente pas deux mais une membrane unique. Par ailleurs, nous avons montré que les protéines SNARE jouent un rôle majeur au cours du trafic intracellulaire de Y. pseudotuberculosis. VAMP3 et VAMP7 sont recrutées de manière séquentielle au niveau de la vacuole de Y. pseudotuberuclosis. VAMP7 va participer au recrutement de LC3 au niveau de la vacuole bactérienne et nous proposons que VAMP3 est un des constituants du check-point permettant l’adressage de la bactérie vers des vacuoles présentant une ou de multiple membranes positives pour LC3. Par la suite, nous nous sommes intéressés à la caractérisation des protéines de la voie autophagique et des endosomes, recrutées au niveau de la vacuole bactérienne à membrane unique et positive pour LC3. Nous avons mis en évidence que les protéines impliquées dans la formation de l’autophagosome et les marqueurs des endosomes précoces sont recrutées au niveau de la vacuole contenant Y. pseudotuberculosis. Cette vacuole positive pour LC3 va en suite acquérir les marqueurs des endosomes tardifs et du lysosome mais n’est pas acidifiée. En outre, nous avons initié des travaux sur un criblage en haut contenu afin d’identifier les partenaires des protéines SNARE et leurs rôles dans le trafic intracellulaire de Y. pseudotuberuclosis. Ces travaux démontrent l’importance de l’analyse de l’ultrastructure des compartiments positifs pour LC3. Ils illustrent comment la bactérie s’adapte à son environnement pour établir sa niche réplicative. Ils présentent enfin l’importance de la régulation de l’autophagie avec la première mise en évidence d’un check-point entre deux voies de compartimentation positives pour LC3 mais morphologiquement différentes
Yersinia pseudotuberculosis is a member of the Enterobacteriaceae family. In human, Y. pseudotuberculosis infection is responsible for enteric and, in rare cases, erythema nodosum. During host colonization, a minor part of Y. pseudotuberculosis presents an intracellular replication step. Y. pseudotuberculosis can replicate inside macrophages by hijacking the autophagy pathway. The bacteria are able to block autophagosome maturation by acidification impairment, which allows to create a replicative niche. The membrane traffic during internalization of Yersinia remains poorly characterized. First, we highlighted that in epithelial cells, Y. pseudotuberculosis replicates mainly in vacuoles positive for LC3, a hallmark of autophagy. Surprisingly, this LC3-positive-vacuole presents only single limiting membrane. Second, we showed that SNARE proteins play a role in Y. pseudotuberculosis intracellular traffic. VAMP3 and VAMP7 are sequentially recruited to Yersinia-containing vacuoles (YCVs). VAMP7 is involved in the LC3 recruitment to YCVs with single- and double-membrane. We proposed that VAMP3 is a component of the molecular checkpoint for bacterial commitment to either single- or double-membrane LC3-positive pathway. Third, we characterized the traffic of endosomal proteins recruited to LC3-positive-YCV with single membrane in epithelial cells. We showed that markers of early endosome and proteins involved in autophagosome formation, are recruited to YCVs during the early stage of infection. Then, the vacuole acquire late endosomal and lysosomal proteins but acidification is not observed. Finally, we initiated a high-content screening approach for the identification of SNARE partners.Overall this work illustrates the importance of LC3-positive compartment ultrastructure analysis. Our result demonstrate how bacterial subvert the molecular machinery of the host in order to create a replicative niche. Finally, we present the importance of autophagy regulation by highlighting for the first times the existence of a molecular checkpoint between two LC3-positive vacuoles with different morphologies

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Asare, Patrick. "An investigation of the Rubicon/LC3 associated phagocytosis (LAP) dysregulation as a therapeutic target in chronic obstructive pulmonary diseases (COPD) and in response to cigarette smoke exposure." Thesis, 2021. https://hdl.handle.net/2440/135321.

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Phagocytic clearance of bacteria and apoptotic cells (a process termed efferocytosis) in COPD is critical to protect against microbial infection and lung tissue injury. The compromised phagocytic capacity of alveolar macrophages in COPD allows bacterial colonisation and is postulated to contribute to the disease severity. However, the precise mechanisms that lead to the macrophage phagocytic dysfunction in COPD remains incompletely understood. LC3-associated phagocytosis (LAP) is a recently discovered cellular event characterised as a critical regulator of effective processing of ingested microbes and apoptotic cells by macrophages. Defective LAP impairs the clearance of pathogens and apoptotic cells by macrophages. Therefore, experiments described in Chapter 2 used novel approaches to measure components of the LAP signalling system including TIM-4, Rubicon, LC3, Atg5, NOX2 in blood monocyte derived macrophages, differentiated THP-1 macrophages and lung tissues of mice exposed to cigarette smoke extract (CSE). Further, the expression of the LAP specific regulator, Rubicon, was examined in bronchoalveolar lavage (BAL)-derived macrophages from COPD patients and healthy controls. The findings of this study showed for the first time that Rubicon/LAP is dysregulated in COPD as a result of CSE exposure. Moreover, the study found that Rubicon inhibition correlated with a defective efferocytosis capacity of alveolar macrophages, confirming a link between LAP inhibition and defective efferocytosis in COPD. Furthermore, this report characterises LAP as a potential therapeutic target for potentiating macrophage efferocytic function in COPD. Modulation of Rubicon/LAP requires a better understanding of the processes that lead to Rubicon/LAP inhibition in COPD. Hence, Chapter 3 of this thesis addressed the mechanisms of Rubicon inhibition by CSE. It was noted that CSE shortens the half-life of Rubicon protein but does not have significant effects on Rubicon mRNA levels. This led to the hypothesis that a protein degradation pathway may contribute to the reduction in Rubicon in macrophages exposed to the factors in cigarette smoke. Further observation that Rubicon degradation could be attenuated by anti-proteases and lysosomal enzyme inhibitors confirmed this hypothesis and demonstrated that lysosomal enzymes may mediate the Rubicon degradation. Moreover, alterations in autophagy or proteasomes did not have significant effects on Rubicon suggesting that Rubicon downregulation by CSE is independent of autophagy or proteasomes.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2022

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Viegas, Michelle. "The role of the endocytic and autophagic molecular machineries in the removal of apoptotic cells." Doctoral thesis, 2014. http://hdl.handle.net/10316/25251.

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Tese de doutoramento em Biociências, apresentada à Faculdade de Ciências e Tecnologia da Universidade de Coimbra
Every day the human body turns over billions of cells ensuring the disposal of unwanted targets that die by apoptosis. The prompt and efficient removal of apoptotic cells by cell line (vascular SMC). The maturation of phagosomes containing dying cells was compared with the processing of phagosomes loaded with IgG-opsonized particles, which are internalized via Fcγ-receptors and are the best characterized phagocytic model. At the present work, we provide evidence that the nature of the cargo modulates the phagocytic response, since phagosomes carrying apoptotic particles reach the lysosomes with a delay when compared to those containing IgG-opsonized particles. Furthermore, for the first time, we have identified some canonical autophagy effectors in phagolysosome formation, suggesting that LC3-Associated Phagocytosis (LAP), a process involved in phagosome maturation, implies more than the phagosomal recruitment of LC3 (Sanjuan et al., 2007). Indeed, experiments performed in bone marrow-derived macrophages from p62-KO mice clearly suggest that p62, despite not being required for LC3 recruitment, is important for phagolysosome biogenesis. In summary, this data will improve our knowledge on the molecular machinery and mechanisms involved in efferocytosis. In the end, we hope to contribute to a better understanding of efferocytosis and the ways to modulate this process, which could culminate with the discovery of therapies that may benefit patients with atherosclerosis and other type of diseases in which efferocytosis is not efficient.phagocytes, referred as to efferocytosis, plays an essential role during development, tissue repair and in the maintenance of homeostasis, triggering an immunological tolerance (Henson and Hume, 2006). On the other hand, defective clearance promote dying cell accumulation, converting harmless apoptotic cells into a risky secondary necrotic state that, eventually, expose self-antigens, which has been linked to the onset of several human disorders, including autoimmunity and chronic inflammatory diseases, such as atherosclerosis (Elliott and Ravichandran, 2010). Atherosclerosis remains the biggest cause of mortality and disabilities worldwide, especially in developing countries. The formation of the atheroma starts with the retention of low-density lipoproteins (LDL) inside the wall of blood vessels, where they become subjected to several chemical modifications. These modified-LDL induce the recruitment of monocyte-derived macrophages, which internalize the deposited fatty material. Over time, these lipid-loaded macrophages are no longer able to process the cholesterol, forming foam-cells that eventually undergo apoptosis. In early stages of atherogenesis, efferocytosis is very efficient; however in advanced lesions this process somehow fails, triggering an inflammatory response that, in turn, recruits more cells, including neighboring smooth muscle cells (SMC). Besides macrophages, SMC, the major cell type in the blood vessels wall, play an essential role by dealing with the dying cell accumulation, thus preventing atheroma progression (Moore and Tabas, 2011). Although many efforts have been done to understand the machinery involved in the recognition of apoptotic cells by phagocytic cells (receptors and ligands), as well as the immune response elicited, very little is known about the intracellular transport of phagosomes containing apoptotic cells and its subsequent digestion into phagolysosomes, the final degradative compartment of the host cell (Hochreiter-Hufford and Ravichandran, 2013). Beyond that, C. elegans has been the model organism in studies of engulfment and degradation of apoptotic cells, which reinforce the need to have more information about the development of this process in mammalian systems. Thus, it is crucial to our understanding, to figure out the causes of the inefficient efferocytosis and how it contributes to the pathogenesis of certain diseases. In this thesis, we have performed a detailed study on the maturation of phagosomes containing human aged red blood cells, our apoptotic cell model, using a mammalian phagocytic

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Stetter, Maurice. "LC3-associated phagocytosis seals the fate of the second polar body in \(Caenorhabditis\) \(elegans\)." Doctoral thesis, 2021. https://doi.org/10.25972/OPUS-23198.

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This work investigates the death and degradation of the second polar body of the nematode C. elegans in order to improve our understanding how pluripotent undifferentiated cells deal with dying cells. With the use of fluorescence microscopy this work demonstrates that both polar bodies loose membrane integrity early. The second polar body has contact to embryonic cells and gets internalized, dependent on the Rac1-ortholog CED-10. The polar body gets degraded via LC3-associated phagocytosis. While lysosome recruitment depends on RAB-7, LC3 does not improve lysosome recruitment but still accelerates polar body degradation. This work establishes the second polar body as a genetic model to study cell death and LC3-associated phagocytosis and has revealed further aspects of phagosome maturation and degradation
Um besser zu verstehen, wie undifferenzierte pluripotente Zellen mit abgestorbenen Zellen umgehen, wird in dieser Dissertation die Phagozytose und der Abbau des 2. Polkörpers der weiblichen Meiose im Fadenwurm C. elegans untersucht. Mithilfe von fluorenzenzmikroskopischen Aufnahmen wird in dieser Arbeit gezeigt, dass beide Polkörper schon früh ihre Membranintegrität verlieren. Der 2. Polkörper, welcher direkten Kontakt zu embryonischen Zellen hat, wird daraufhin mithilfe des Rac1-Orthologs CED-10 phagozytiert. Es wird gezeigt, dass es sich bei dem Abbauprozess um LC3-assoziierte Phagozytose handelt. Die RAB-7 GTPase ist notwendig für die Rekrutierung von Lysosomen, während LC3 darauf keinen Einfluss hat, aber trotzdem den Abbau des Polkörpers beschleunigt. Mit dieser Arbeit konnte ein genetisches Modell für die Erforschung von Zelltod und der LC3-assoziierten Phagozytose entwickelt werden und weitere Aspekte der Phagosomreifung und des -abbaus aufgedeckt werden

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Частини книг з теми "LC3 associated phagocytosis (LAP)"

Ligeon, Laure-Anne, Susana Romao, and Christian Münz. "Analysis of LC3-Associated Phagocytosis and Antigen Presentation." In Methods in Molecular Biology, 145–68. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6581-6_10.

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Jacquin, Elise, Katherine Fletcher, and Oliver Florey. "Imaging Noncanonical Autophagy and LC3-Associated Phagocytosis in Cultured Cells." In Methods in Molecular Biology, 295–303. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8873-0_19.

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Holownia, A., A. Niechoda, J. Lachowicz, E. Golabiewska, and U. Baranowska. "Phagocytosis and Autophagy in THP-1 Cells Exposed to Urban Dust: Possible Role of LC3-Associated Phagocytosis and Canonical Autophagy." In Advances in Medicine and Medical Research, 55–63. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/5584_2018_323.

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Wong, Sing-Wai, Sandeep Upadhyay, and Jennifer Martinez. "LC3-associated phagocytosis." In Non-Canonical Autophagy, 69–91. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820538-9.00005-3.

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Cunha, Larissa D., and Jennifer Martinez. "Autophagy and LC3-Associated Phagocytosis Mediate the Innate Immune Response." In Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging, 303–19. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-805420-8.00016-0.

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Тези доповідей конференцій з теми "LC3 associated phagocytosis (LAP)"

Asare, P. F., E. Roscioli, P. R. Hurtado, H. B. Tran, S. Maiolo, and S. Hodge. "THP-1 Macrophages Exposed to the Factors in Cigarette Smoke Exhibit Dysregulation of LC3-Associated Phagocytosis (LAP)." 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.a4752.

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Green, Douglas R. "Abstract IA13: LC3-associated phagocytosis in inflammation and anticancer immunity." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-ia13.

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Moore, Jamie Aaron, Jayna J. Mistry, Charlotte Hellmich, Aisha Jibril, Tom Wileman, Angela Collins, Kristian M. Bowles, and Stuart A. Rushworth. "Abstract 2752: LC3-associated phagocytosis in bone marrow macrophages suppresses AML progression through TIM-4 mediated STING activation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2752.

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