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The Drosophila melanogaster host model.

Igboin CO, Griffen AL, Leys EJ - J Oral Microbiol (2012)

Bottom Line: These studies have revealed that there is a remarkable conservation of bacterial pathogenesis and host defence mechanisms between higher host organisms and Drosophila.This review presents an in-depth discussion of the Drosophila immune response, the Drosophila killing model, and the use of the model to examine bacterial-host interactions.The recent introduction of the Drosophila model into the oral microbiology field is discussed, specifically the use of the model to examine Porphyromonas gingivalis-host interactions, and finally the potential uses of this powerful model system to further elucidate oral bacterial-host interactions are addressed.

View Article: PubMed Central - PubMed

Affiliation: Division of Oral Biology, College of Dentistry, The Ohio State University, Columbus, Ohio, USA.

ABSTRACT
The deleterious and sometimes fatal outcomes of bacterial infectious diseases are the net result of the interactions between the pathogen and the host, and the genetically tractable fruit fly, Drosophila melanogaster, has emerged as a valuable tool for modeling the pathogen-host interactions of a wide variety of bacteria. These studies have revealed that there is a remarkable conservation of bacterial pathogenesis and host defence mechanisms between higher host organisms and Drosophila. This review presents an in-depth discussion of the Drosophila immune response, the Drosophila killing model, and the use of the model to examine bacterial-host interactions. The recent introduction of the Drosophila model into the oral microbiology field is discussed, specifically the use of the model to examine Porphyromonas gingivalis-host interactions, and finally the potential uses of this powerful model system to further elucidate oral bacterial-host interactions are addressed.

No MeSH data available.


Related in: MedlinePlus

Survival curves of adult, female Drosophila infected with P. gingivalis and other bacterial species. E. coli DH5α (pink curve), P. aeruginosa strain PA01 (blue curve), P. gingivalis strain W83 (red curve), and vehicular control (yellow curve) (63).
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Figure 0002: Survival curves of adult, female Drosophila infected with P. gingivalis and other bacterial species. E. coli DH5α (pink curve), P. aeruginosa strain PA01 (blue curve), P. gingivalis strain W83 (red curve), and vehicular control (yellow curve) (63).

Mentions: Using a septic injury route of infection, P. gingivalis was pathogenic to Drosophila, in a dose-dependent manner, with an intermediate level of pathogenicity between the non-pathogenic E. coil DH5-alpha and the highly pathogenic P. aeruginosa PA01 (Fig. 2). A comparison of clinically prevalent heteroduplex type strains of P. gingivalis revealed that all of the strains were virulent to some degree in Drosophila and that the highly disease-associated type strain, W83, was also the most pathogenic in the flies. P. gingivalis colony-forming unit levels did not increase in the Drosophila; however, the bacterium was able to persist in the flies up to 60 h postinfection. The relatively low temperature at which the infected flies were incubated (30°C), in addition to the oxygen rich environment of the hemolymph likely contribute to the inability of P. gingivalis to multiply in the host. However, P. gingivalis is aerotolerant and can survive exposure to air for up to 5 h without any loss in viability, which likely accounted for the bacterium's ability to persist in the Drosophila postinfection. P. gingivalis killing of Drosophila was not due to overt destruction of the fly tissues or a high bacterial burden as was observed with other pathogens, rather the observation that both live and heat-killed P. gingivalis effectively killed Drosophila suggested that the pathology may be due primarily to the host's own exaggerated immune response. Futher experiments are warranted to determine the exact cause of death of P. gingivalis-infected Drosophila, for example, in vivo RNAi could be used to dampen Drosophila immune responses and assess whether fly survival of P. gingivalis infection is enhanced as a result.


The Drosophila melanogaster host model.

Igboin CO, Griffen AL, Leys EJ - J Oral Microbiol (2012)

Survival curves of adult, female Drosophila infected with P. gingivalis and other bacterial species. E. coli DH5α (pink curve), P. aeruginosa strain PA01 (blue curve), P. gingivalis strain W83 (red curve), and vehicular control (yellow curve) (63).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3285217&req=5

Figure 0002: Survival curves of adult, female Drosophila infected with P. gingivalis and other bacterial species. E. coli DH5α (pink curve), P. aeruginosa strain PA01 (blue curve), P. gingivalis strain W83 (red curve), and vehicular control (yellow curve) (63).
Mentions: Using a septic injury route of infection, P. gingivalis was pathogenic to Drosophila, in a dose-dependent manner, with an intermediate level of pathogenicity between the non-pathogenic E. coil DH5-alpha and the highly pathogenic P. aeruginosa PA01 (Fig. 2). A comparison of clinically prevalent heteroduplex type strains of P. gingivalis revealed that all of the strains were virulent to some degree in Drosophila and that the highly disease-associated type strain, W83, was also the most pathogenic in the flies. P. gingivalis colony-forming unit levels did not increase in the Drosophila; however, the bacterium was able to persist in the flies up to 60 h postinfection. The relatively low temperature at which the infected flies were incubated (30°C), in addition to the oxygen rich environment of the hemolymph likely contribute to the inability of P. gingivalis to multiply in the host. However, P. gingivalis is aerotolerant and can survive exposure to air for up to 5 h without any loss in viability, which likely accounted for the bacterium's ability to persist in the Drosophila postinfection. P. gingivalis killing of Drosophila was not due to overt destruction of the fly tissues or a high bacterial burden as was observed with other pathogens, rather the observation that both live and heat-killed P. gingivalis effectively killed Drosophila suggested that the pathology may be due primarily to the host's own exaggerated immune response. Futher experiments are warranted to determine the exact cause of death of P. gingivalis-infected Drosophila, for example, in vivo RNAi could be used to dampen Drosophila immune responses and assess whether fly survival of P. gingivalis infection is enhanced as a result.

Bottom Line: These studies have revealed that there is a remarkable conservation of bacterial pathogenesis and host defence mechanisms between higher host organisms and Drosophila.This review presents an in-depth discussion of the Drosophila immune response, the Drosophila killing model, and the use of the model to examine bacterial-host interactions.The recent introduction of the Drosophila model into the oral microbiology field is discussed, specifically the use of the model to examine Porphyromonas gingivalis-host interactions, and finally the potential uses of this powerful model system to further elucidate oral bacterial-host interactions are addressed.

View Article: PubMed Central - PubMed

Affiliation: Division of Oral Biology, College of Dentistry, The Ohio State University, Columbus, Ohio, USA.

ABSTRACT
The deleterious and sometimes fatal outcomes of bacterial infectious diseases are the net result of the interactions between the pathogen and the host, and the genetically tractable fruit fly, Drosophila melanogaster, has emerged as a valuable tool for modeling the pathogen-host interactions of a wide variety of bacteria. These studies have revealed that there is a remarkable conservation of bacterial pathogenesis and host defence mechanisms between higher host organisms and Drosophila. This review presents an in-depth discussion of the Drosophila immune response, the Drosophila killing model, and the use of the model to examine bacterial-host interactions. The recent introduction of the Drosophila model into the oral microbiology field is discussed, specifically the use of the model to examine Porphyromonas gingivalis-host interactions, and finally the potential uses of this powerful model system to further elucidate oral bacterial-host interactions are addressed.

No MeSH data available.


Related in: MedlinePlus