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The role of Intelectin-2 in resistance to Ascaris suum lung larval burdens in susceptible and resistant mouse strains

Published online by Cambridge University Press:  24 February 2011

CHRISTINA DOLD*
Affiliation:
Department of Zoology, School of Natural Sciences, Trinity College, Dublin 2, Ireland
ALAN D. PEMBERTON
Affiliation:
Division of Veterinary Clinical Studies, University of Edinburgh, Easter Bush Veterinary Centre, Roslin, Midlothian EH25 9RG, UK
PETER STAFFORD
Affiliation:
Department of Zoology, School of Natural Sciences, Trinity College, Dublin 2, Ireland
CELIA V. HOLLAND
Affiliation:
Department of Zoology, School of Natural Sciences, Trinity College, Dublin 2, Ireland
JERZY M. BEHNKE
Affiliation:
School of Biology, University of Nottingham, University Park, Nottingham NG7 2RD, UK
*
*Corresponding author: Department of Zoology, School of Natural Sciences, Trinity College, Dublin 2, Ireland. Tel: +353 1 896 2194. Fax: +353 1 677 8094. E-mail: [email protected]

Summary

The underlying mechanism of predisposition to Ascaris infection is not yet understood but host genetics are thought to play a fundamental role. We investigated the association between the Intelectin-2 gene and resistance in F2 mice derived from mouse strains known to be susceptible and resistant to infection. Ascaris larvae were isolated from murine lungs and the number of copies of the Intelectin-2 gene was determined in F2 mice. Intelectin-2 gene copy number was not significantly linked to larval burden. In a pilot experiment, the response to infection in parental mice of both sexes was observed in order to address the suitablity of female F2 mice. No overall significant sex effect was detected. However, a divergence in resistance/susceptibility status was observed between male and, female hybrid offspring. The responsiveness to Ascaris in mice is likely to be controlled by multiple genes and, despite a unique absence from the susceptible C57BL/6j strain, the Intelectin-2 gene does not play a significant role in resistance. The observed intra-strain variation in larval burden requires further investigation but we hypothesize that it stems from social/dominance hierarchies created by the presence of female mice and possibly subsequent hormonal perturbations that modify the intensity of the immune response.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2011

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References

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