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Review
. 2005 Jul;73(7):3833-41.
doi: 10.1128/IAI.73.7.3833-3841.2005.

Worms and flies as genetically tractable animal models to study host-pathogen interactions

Eleftherios Mylonakis  1 , Alejandro Aballay
Affiliations
Review

Worms and flies as genetically tractable animal models to study host-pathogen interactions

Eleftherios Mylonakis et al. Infect Immun. 2005 Jul.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Comparison of the D. melanogaster innate immunity pathway with homolog pathways in C. elegans and mammals. In mammals and D. melanogaster, Toll-like receptors are crucial in the recognition of microbial pathogens prior to the elicitation of innate immune responses. The C. elegans Tol-1 receptor is apparently not involved in this process. The intracellular TIR domain of Toll interacts with a similar domain contained in the MyD88 conserved protein. In mammals, this leads to the activation of both MAPKs and NF-κB that ultimately activates the innate immune system. Similarly, Toll activation triggers innate immunity in D. melanogaster through the activation of the NF-κB-like transcription factors Dorsal and DIF. Upon the recognition of microbial pathogens, a C. elegans receptor(s) yet to be identified activates innate immunity through a Tir-1/MAPK signaling pathway. As in mammals, C. elegans defense responses involve the activation of microbial killing pathways and apoptotic pathways. Although caspases are required for the activation of innate immunity in D. melanogaster, an apoptotic defense response has not yet been reported.
FIG. 2.
FIG. 2.
Genetic analysis identified innate immunity pathways required for proper defense responses in flies and nematodes. (A) D. melanogaster F3 male mutagenized larvae carrying the transgene dipt::lacZ were inoculated with a diluted culture of E. coli. After 2.5 h, the larvae were inspected for melanization at the wound site and then the β-galactosidase activity was evaluated to isolate mutants exhibiting an impaired defense response. (B) An EMS-mutagenized F2 population of worms was transferred to agar plates seeded with P. aeruginosa to identify C. elegans mutants impaired in defense response. Because wild-type animals infected with P. aeruginosa typically start to die at approximately 34 h, dead mutant animals were isolated during a period of 16 to 30 h. Because C. elegans eggs are not infected by bacterial pathogens, the candidate mutants were recovered by transferring individual dead worms containing their brood to plates seeded with nonpathogenic E. coli.
FIG. 3.
FIG. 3.
Expression of bacterial virulence factors in C. elegans cells diminishes innate immunity. A genetic analysis indicates that S. enterica TTSS-related genes are required for full virulence in C. elegans. To confirm that effector proteins secreted through SPI-1 TTSS affect C. elegans innate immunity, SptP was directly expressed in the intestinal cells of nematodes. The intestinal expression of SptP diminishes C. elegans innate immunity apparently by preventing the activation of MAPK PMK-1. It remains unknown whether the SptP GTPase activating protein activity, the tyrosine phosphatase activity, or both are required for the downregulation of MAPK PMK-1.
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