Drosophila as a Model Organism in Host–Pathogen Interaction Studies

Younes, Salma; Al-Sulaiti, Asma; Nasser, Elham Abdulwahab Ahmed; Najjar, Hoda; Kamareddine, Layla

doi:10.3389/fcimb.2020.00214

Cited by 49 publications

(39 citation statements)

References 169 publications

(186 reference statements)

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“…A fruit fly serves as an important model organism in host-pathogen interaction studies [87]. Although details on the relationship between the microbiota and pathogen virulence are still emerging, studies clearly designate a role of commensals in host resistance to infection.…”

Section: The Role Of the Gut Microbiota In Fruit Fly-pathogen Interactionsmentioning

confidence: 99%

The Microbiota and Gut-Related Disorders: Insights from Animal Models

Kamareddine

Najjar

Sohail

et al. 2020

Cells

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Over the past decade, the scientific committee has called for broadening our horizons in understanding host–microbe interactions and infectious disease progression. Owing to the fact that the human gut harbors trillions of microbes that exhibit various roles including the production of vitamins, absorption of nutrients, pathogen displacement, and development of the host immune system, particular attention has been given to the use of germ-free (GF) animal models in unraveling the effect of the gut microbiota on the physiology and pathophysiology of the host. In this review, we discuss common methods used to generate GF fruit fly, zebrafish, and mice model systems and highlight the use of these GF model organisms in addressing the role of gut-microbiota in gut-related disorders (metabolic diseases, inflammatory bowel disease, and cancer), and in activating host defense mechanisms and amending pathogenic virulence.

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Section: The Role Of the Gut Microbiota In Fruit Fly-pathogen Interactionsmentioning

confidence: 99%

The Microbiota and Gut-Related Disorders: Insights from Animal Models

Kamareddine

Najjar

Sohail

et al. 2020

Cells

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“…L. pneumophila is primarily found in aquatic environments and has evolved to invade and proliferate within diverse amoebae species [ 46 ], but upon transmission to humans, causes pneumonia [ 43 , 47 , 48 , 49 ]. This bacterium has evolved to bypass the default endosomal–lysosomal pathway within eukaryotic cells and generates a replicative vacuole derived from the endoplasmic reticulum, termed the Legionella -containing vacuole, (LCV) [ 50 , 51 , 52 , 53 ]. Upon uptake by coiling phagocytosis by host cells [ 54 ], this bacterium immediately begins to modulate a plethora of host cell processes through injection of a complex tool box of over 320 different effector proteins through the Dot/Icm type IVB secretion system, which functions as a nanosyringe [ 55 , 56 ].…”

Section: Introductionmentioning

confidence: 99%

Evolution and Adaptation of Legionella pneumophila to Manipulate the Ubiquitination Machinery of Its Amoebae and Mammalian Hosts

Price

Kwaik

2021

Biomolecules

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The ubiquitin pathway is highly conserved across the eukaryotic domain of life and plays an essential role in a plethora of cellular processes. It is not surprising that many intracellular bacterial pathogens often target the essential host ubiquitin pathway. The intracellular bacterial pathogen Legionella pneumophila injects into the host cell cytosol multiple classes of classical and novel ubiquitin-modifying enzymes that modulate diverse ubiquitin-related processes in the host cell. Most of these pathogen-injected proteins, designated as effectors, mimic known E3-ubiquitin ligases through harboring F-box or U-box domains. The classical F-box effector, AnkB targets host proteins for K48-linked polyubiquitination, which leads to excessive proteasomal degradation that is required to generate adequate supplies of amino acids for metabolism of the pathogen. In contrast, the SidC and SdcA effectors share no structural similarity to known eukaryotic ligases despite having E3-ubiquitin ligase activity, suggesting that the number of E3-ligases in eukaryotes is under-represented. L. pneumophila also injects into the host many novel ubiquitin-modifying enzymes, which are the SidE family of effectors that catalyze phosphoribosyl-ubiquitination of serine residue of target proteins, independently of the canonical E1-2-3 enzymatic cascade. Interestingly, the environmental bacterium, L. pneumophila, has evolved within a diverse range of amoebal species, which serve as the natural hosts, while accidental transmission through contaminated aerosols can cause pneumonia in humans. Therefore, it is likely that the novel ubiquitin-modifying enzymes of L. pneumophila were acquired by the pathogen through interkingdom gene transfer from the diverse natural amoebal hosts. Furthermore, conservation of the ubiquitin pathway across eukaryotes has enabled these novel ubiquitin-modifying enzymes to function similarly in mammalian cells. Studies on the biological functions of these effectors are likely to reveal further novel ubiquitin biology and shed further lights on the evolution of ubiquitin.

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“…A model that can be used in large numbers and have fewer ethical concerns would be of particular importance during the initial phases of research. Due to economic, technical, and ethical concerns associated with the use of vertebrate animals, scientists are turning toward invertebrate animal models such as Caenorhabditis elegans 19–21 , Drosophila melanogaster 22–24 , Galleria mellonella 25–27 and Bombyx mori 23–30 for large scale screenings. While accurate dose administration in C. elegans and D. melanogaster is difficult due to their small size, the use of G. mellonella is challenging due to its faster locomotion.…”

Section: Introductionmentioning

confidence: 99%

Silkworm model forBacillus anthracisinfection and virulence determination

Paudel

Furuta

Higashi

2021

Preprint

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Bacillus anthracis is an obligate pathogen and a causative agent of anthrax. Its major virulence factors are plasmid-coded; however, recent studies have revealed chromosome-encoded virulence factors, indicating that the current understanding of its virulence mechanism is elusive and needs further investigation. In this study, we established a silkworm (Bombyx mori) infection model of B. anthracis Sterne. We showed that silkworms were killed by B. anthracis and cured of the infection when administered with antibiotics. We quantitatively determined the lethal dose of the bacteria that kills 50% larvae and effective doses of antibiotics that cure 50% infected larvae. Furthermore, we demonstrated that B. anthracis mutants with disruption in virulence genes such as pagA, lef, and atxA had attenuated silkworm-killing ability and reduced colonization in silkworm hemolymph. The silkworm infection model established in this study can be utilized in large-scale infection experiments to identify novel virulence determinants and develop novel therapeutic options against B. anthracis infections.

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Drosophila as a Model Organism in Host–Pathogen Interaction Studies

Cited by 49 publications

References 169 publications

The Microbiota and Gut-Related Disorders: Insights from Animal Models

The Microbiota and Gut-Related Disorders: Insights from Animal Models

Evolution and Adaptation of Legionella pneumophila to Manipulate the Ubiquitination Machinery of Its Amoebae and Mammalian Hosts

Silkworm model forBacillus anthracisinfection and virulence determination

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