Exploration of host-pathogen interactions using Listeria monocytogenes and Drosophila melanogaster

Mansfield, Bryce E.; Dionne, Marc S.; Schneider, David; Freitag, Nancy E.

doi:10.1046/j.1462-5822.2003.00329.x

Cited by 168 publications

(151 citation statements)

References 40 publications

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“…Insects have been employed to assess the relative pathogenicity of bacteria [19], fungi [20] and parasites [21] and positive correlations with results from murine studies have been demonstrated in C. albicans [22] and Pseudomonas aeruginosa [23].…”

Section: U N C O R R E C T E D P R O O Fmentioning

confidence: 99%

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Bergin

Murphy

Keenan

et al. 2006

Microbes and Infection

132

130

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Pre-exposure of the larvae of Galleria mellonella to Candida albicans or Saccharomyces cerevisiae protects against a subsequent infection with 10 6 C. albicans cells. This protection can also be induced by exposing larvae to glucan or laminarin prior to the administration of the potentially lethal inoculum. Analysis of the expression of genes coding for galiomicin, a defensin in G. mellonella, a cysteine-rich antifungal peptide gallerimycin, an iron-binding protein transferrin and an inducible metalloproteinase inhibitor (IMPI) from G. mellonella demonstrated increased expression, which is at its highest after 24 h of the initial inoculum. Examination of the expression of proteins in the insect haemolymph using 2D electrophoresis and MALDI TOF analysis revealed an increased expression of a number of proteins associated with the insect immune response to infection 24 h after the initial exposure. This study demonstrates that the larvae of G. mellonella can withstand a lethal inoculum of C. albicans if pre-exposed to a non-lethal dose of yeast or polysaccharide 24 h previously which is mediated by increased expression of a number of antimicrobial peptides and the appearance of a number of peptides in the challenged larvae.

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Section: U N C O R R E C T E D P R O O Fmentioning

confidence: 99%

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Bergin

Murphy

Keenan

et al. 2006

Microbes and Infection

132

130

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“…The insect immune response bears a number of similarities to the innate immune response of mammals and as a result various insects have been utilised for assessing the pathogenicity of bacterial [2] and fungal isolates [3] and for assessing the efficacy of a variety of antimicrobial drugs. Positive correlations between the virulence of microbial pathogens in insects and mammals [4,5] have been established and the use of insects for screening microbial mutants or antimicrobial drugs is now recognized as a valuable approach to reduce the need to use mammals for this type of testing [6].…”

Section: Introductionmentioning

confidence: 99%

Physical stress primes the immune response of Galleria mellonella larvae to infection by Candida albicans

Mowlds

Barron

Kavanagh

2008

Microbes and Infection

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Larvae of the greater wax moth (Galleria mellonella) that had been subjected to physical stress by shaking in cupped hands for 2 min showed reduced susceptibility to infection by Candida albicans when infected 24 h after the stress event. Physically stressed larvae demonstrated an increase in haemocyte density and elevated mRNA levels of galiomicin and an inducible metalloproteinase inhibitor (IMPI ) but not transferrin or gallerimycin. In contrast, previous work has demonstrated that microbial priming of larvae resulted in the induction of all four genes. Examination of the expression of proteins in the insect haemolymph using 2D electrophoresis and MALDI TOF analysis revealed an increase in the intensity of a number of peptides showing some similarities with proteins associated with the insect immune response to infection. This study demonstrates that non-lethal physical stress primes the immune response of G. mellonella and this is mediated by elevated haemocyte numbers, increased mRNA levels of genes coding for two antimicrobial peptides and the appearance of novel peptides in the haemolymph. This work demonstrates that physical priming increases the insect immune response but the mechanism of this priming is different to that induced by low level exposure to microbial pathogens.

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“…Recently, Drosophila S2 cells have been established as a suitable host model for bacterial infections (11)(12)(13). These macrophage-like cells were shown to behave similarly to mammalian cells in in vitro infection assays using L. monocytogenes.…”

mentioning

confidence: 99%

Use of RNA interference inDrosophilaS2 cells to identify host pathways controlling compartmentalization of an intracellular pathogen

Cheng

Viala

Stuurman

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

114

109

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Three genome-wide RNA interference screens were performed in Drosophila S2 cells to dissect the contribution of host processes to Listeria monocytogenes entry, vacuolar escape, and intracellular growth. Among the 116 genes identified, several host pathways previously unrecognized as playing a role in listerial pathogenesis were identified: knockdowns affecting vacuolar trafficking to and from the multivesicular body bypassed the requirement for the essential pore-forming toxin listeriolysin O in mediating escape from phagocytic vacuoles and knockdowns affecting either subunit of serine palmitoyltransferase, a key enzyme in ceramide and sphingolipid biosynthesis, enhanced the toxicity of listeriolysin O expressed in the host cell cytosol, leading to lack of appropriate toxin activity compartmentalization and host cell death. Genomewide RNA interference screens using Drosophila S2 cells proved to be a powerful approach to dissect host-pathogen interactions.Listeria monocytogenes ͉ listeriolysin O ͉ multivesicular bodies ͉ serine palmitoyltransferase I nfectious diseases caused by intracellular pathogens are responsible for an enormous amount of worldwide morbidity and mortality. These pathogens exploit the basic processes of host cells to establish their intracellular niche (1). Listeria monocytogenes, a facultative intracellular Gram-positive bacterial pathogen, thrives in the cytosol of host cells. The intracellular life cycle of L. monocytogenes has been well defined (2) and can be summarized as follows. Bacteria enter cells by either phagocytosis or bacteria-mediated internalization. Subsequent to internalization, the bacteria produce a cholesterol-dependent pore-forming cytolysin, termed listeriolysin O (LLO), and two phospholipases C (PLCs) that mediate rupture of the resulting phagosome, thereby allowing bacteria access to the rich milieu of the host cytosol. Once in the cytosol, bacteria grow rapidly and exploit a host system of actin-based motility to move intracellularly and spread from cell to cell. Mutants lacking LLO cannot escape from the phagosome, whereas those lacking PLCs are partially defective in escape. In some mammalian epithelial cells, however, a requirement for LLO can be bypassed, and in that case, PLCs are required for vacuolar escape (3, 4). Nevertheless, LLO is absolutely required for pathogenicity and is essential in the vast majority of cells analyzed. However, LLO is a doubleedged sword that can kill the host cell if expressed inappropriately. Mutations affecting its acidic pH optimum or in a PESTlike sequence result in inappropriate LLO expression in the cytosol, leading to plasma membrane damage, premature cell death, and severe attenuation in experimental listeriosis (5-7).Although much has been learned about the cellular microbiology of L. monocytogenes infection, the characterization of host processes contributing to pathogenesis has been hampered by the lack of tools for whole-genome genetic manipulations of the host. Many unanswered questions remain, such as how do bacteria e...

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Exploration of host-pathogen interactions using Listeria monocytogenes and Drosophila melanogaster

Cited by 168 publications

References 40 publications

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Pre-exposure to yeast protects larvae of Galleria mellonella from a subsequent lethal infection by Candida albicans and is mediated by the increased expression of antimicrobial peptides

Physical stress primes the immune response of Galleria mellonella larvae to infection by Candida albicans

Use of RNA interference inDrosophilaS2 cells to identify host pathways controlling compartmentalization of an intracellular pathogen

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