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In-Depth Information
larval migration and the accompanying host response, and this could be
extended to differing parasite genotypes within a species. Nesjum et al.
88
infected pigs with A. suum worms with unique mtDNA haplotypes and
revealed an uneven distribution of the different genotypes within the host
intestine. The mouse model could also be a useful and cost-effective
model system to explore the host and parasite transcriptome. As des-
cribed by Jex et al.
89
(see Chapter 11), the extensive and complex
migration undertaken by Ascaris requires tightly regulated transcriptional
changes in the parasite. Transcription profiles of infective L3 larvae from
eggs and from the liver and lungs revealed various secreted peptidases
linked to tissue migration and degradation during feeding and/or
migration. Proteinases secreted by Ascaris larvae are known to be inhib-
itable by antibody,
90
and it would be interesting to discover whether
proteinase inhibitors released by the liver during inflammatory and acute
phase responses also inhibit them, and whether variation in the intensity
and quality of secreted host proteinase inhibitors in turn is linked to the
differential success of migrating larvae in resistant and susceptible strains
of mice.
To conclude, the use of an animal model that provides two contrasting
response phenotypes as reflected in two inbred mouse strains is an asset
in teasing apart the mechanisms that confer resistance and predisposi-
tion to light and heavy Ascaris infection, and there is still much yet to be
done to fully understand the nature of this genetic resistance. Focus
upon the innate cellular immune response to migrating larvae within the
liver would seem to be a particularly fruitful line of enquiry. Once
detailed knowledge of the cellular hepatic response at the molecular
level is available, this may enhance our ability to develop immuno-
modulatory therapies to elicit resistance to infection in both people and
pigs. More generally, increasing our knowledge of larval ascariasis will
contribute to the development of intervention strategies for early stages
of the life-cycle, aimed at preventing parasite establishment and thus
chronic disease.
Acknowledgments
We thank Kieran Dold for creating
Figure 5.1
. Celia Holland acknowledges the financial
support of the Irish Research Council and Science Foundation Ireland.
References
1. Sprent JF. The life cycles of nematodes in the family Ascarididae Blanchard 1896.
J Parasitol 1954;40:608
17.
2. Maung M. The occurrence of the second moult of Ascaris lumbricoides and Ascaris suum.
In J Parasitol 1978;8:371
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