Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections

Modeling human infectious diseases using the early life stages of zebrafish provides unprecedented opportunities for visualizing and studying the interaction between pathogens and phagocytic cells of the innate immune system. Intracellular pathogens use phagocytes or other host cells, like gut epith...

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Main Authors: Salomé Muñoz-Sánchez, Michiel van der Vaart, Annemarie H. Meijer
Format: Article
Language:English
Published: MDPI AG 2020-10-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/9/11/2372
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author Salomé Muñoz-Sánchez
Michiel van der Vaart
Annemarie H. Meijer
author_facet Salomé Muñoz-Sánchez
Michiel van der Vaart
Annemarie H. Meijer
author_sort Salomé Muñoz-Sánchez
collection DOAJ
description Modeling human infectious diseases using the early life stages of zebrafish provides unprecedented opportunities for visualizing and studying the interaction between pathogens and phagocytic cells of the innate immune system. Intracellular pathogens use phagocytes or other host cells, like gut epithelial cells, as a replication niche. The intracellular growth of these pathogens can be counteracted by host defense mechanisms that rely on the autophagy machinery. In recent years, zebrafish embryo infection models have provided in vivo evidence for the significance of the autophagic defenses and these models are now being used to explore autophagy as a therapeutic target. In line with studies in mammalian models, research in zebrafish has shown that selective autophagy mediated by ubiquitin receptors, such as p62, is important for host resistance against several bacterial pathogens, including <i>Shigella flexneri</i>, <i>Mycobacterium marinum</i>, and <i>Staphylococcus aureus</i>. Furthermore, an autophagy related process, Lc3-associated phagocytosis (LAP), proved host beneficial in the case of <i>Salmonella</i> Typhimurium infection but host detrimental in the case of <i>S. aureus</i> infection, where LAP delivers the pathogen to a replication niche. These studies provide valuable information for developing novel therapeutic strategies aimed at directing the autophagy machinery towards bacterial degradation.
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spelling doaj.art-bcb9f69f2fbb40de808d5657389b48ba2023-11-20T18:59:04ZengMDPI AGCells2073-44092020-10-01911237210.3390/cells9112372Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial InfectionsSalomé Muñoz-Sánchez0Michiel van der Vaart1Annemarie H. Meijer2Institute of Biology Leiden, Leiden University, Einsteinweg 55, 2333 CC Leiden, The NetherlandsInstitute of Biology Leiden, Leiden University, Einsteinweg 55, 2333 CC Leiden, The NetherlandsInstitute of Biology Leiden, Leiden University, Einsteinweg 55, 2333 CC Leiden, The NetherlandsModeling human infectious diseases using the early life stages of zebrafish provides unprecedented opportunities for visualizing and studying the interaction between pathogens and phagocytic cells of the innate immune system. Intracellular pathogens use phagocytes or other host cells, like gut epithelial cells, as a replication niche. The intracellular growth of these pathogens can be counteracted by host defense mechanisms that rely on the autophagy machinery. In recent years, zebrafish embryo infection models have provided in vivo evidence for the significance of the autophagic defenses and these models are now being used to explore autophagy as a therapeutic target. In line with studies in mammalian models, research in zebrafish has shown that selective autophagy mediated by ubiquitin receptors, such as p62, is important for host resistance against several bacterial pathogens, including <i>Shigella flexneri</i>, <i>Mycobacterium marinum</i>, and <i>Staphylococcus aureus</i>. Furthermore, an autophagy related process, Lc3-associated phagocytosis (LAP), proved host beneficial in the case of <i>Salmonella</i> Typhimurium infection but host detrimental in the case of <i>S. aureus</i> infection, where LAP delivers the pathogen to a replication niche. These studies provide valuable information for developing novel therapeutic strategies aimed at directing the autophagy machinery towards bacterial degradation.https://www.mdpi.com/2073-4409/9/11/2372innate immunityautophagyLAPDram1p62Optn
spellingShingle Salomé Muñoz-Sánchez
Michiel van der Vaart
Annemarie H. Meijer
Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
Cells
innate immunity
autophagy
LAP
Dram1
p62
Optn
title Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
title_full Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
title_fullStr Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
title_full_unstemmed Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
title_short Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections
title_sort autophagy and lc3 associated phagocytosis in zebrafish models of bacterial infections
topic innate immunity
autophagy
LAP
Dram1
p62
Optn
url https://www.mdpi.com/2073-4409/9/11/2372
work_keys_str_mv AT salomemunozsanchez autophagyandlc3associatedphagocytosisinzebrafishmodelsofbacterialinfections
AT michielvandervaart autophagyandlc3associatedphagocytosisinzebrafishmodelsofbacterialinfections
AT annemariehmeijer autophagyandlc3associatedphagocytosisinzebrafishmodelsofbacterialinfections