Allen, J.E.

Babayan, S.

Bünger, L.

Coltherd, J.C.

Houdijk, J.G.M.

Kyriazakis, I.

English

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       Coltherd, J.C., Babayan, S., Bünger, L., Kyriazakis, I., Allen, J.E., and Houdijk, J.G.M. (2009) Immune responses to macroparasites are sensitive to the interaction between genetic growth potential and protein nutrition in mice. Proceedings of the Nutrition Society, 68 (OCE3). E101. ISSN 0029-665  Copyright © 2009 Cambridge University Press  A copy can be downloaded for personal non-commercial research or study, without prior permission or charge   The content must not be changed in any way or reproduced in any format or medium without the formal permission of the copyright holder(s)   When referring to this work, full bibliographic details must be given      http://eprints.gla.ac.uk/81215/       Deposited on:  13 September 2013          Enlighten – Research publications by members of the University of Glasgow http://eprints.gla.ac.uk Irish Section of The Nutrition Society, 17–19 June 2009Immune responses to macroparasites are sensitive to the interactionbetween genetic growth potential and protein nutrition in miceJ. C. Coltherd1, S. Babayan2, L. Bu¨nger3, I. Kyriazakis1,4, J. E. Allen2 and J. G. M. Houdijk11Animal Health, SAC, Edinburgh EH9 3JG, UK, 2IIIR, Ashworth Laboratories, Edinburgh EH9 3JT, UK,3Animal Breeding and Genetics Team, SAC, Edinburgh EH9 3JG, UK and 4Veterinary Faculty, University of Thessaly,43100 Karditsa, GreeceAnimals selected narrowly for increased production traits may be penalised more from pathogen challenges than their unselectedcounterparts. These genetic correlations between production and immune traits could be based on changes in the allocation of scarceresources to immune functions. This possibility is addressed in mice that have been divergently selected over thirty-eight generations for high(ROH) and low (ROL) body weight at 42 d of age(1). Infection with a gastrointestinal parasite in ROH mice results in a greater penaltyon resilience (body weight and food intake) and resistance (parasite egg numbers and worm burden) than in ROL mice(2). This penalty onresilience is sensitive to protein nutrition, but the expected sensitivity of resistance to protein nutrition(3) is not significant. The aim of thecurrent study was to assess host immune responses that may underlie interactive effects of genetic potential and protein nutrition on resistanceto parasites.In a 2 · 2 · 2 design, individually-housed male ROL and ROH mice were fed ad libitum diets with either 40 (LP) or 230 (HP) g crudeprotein (N · 6.25)/kg and either sham infected or infected with Heligmosomoides bakeri larvae at 32 d of age (n 6). Feed intake and bodyweight were assessed twice weekly for 28 d when worm burdens, cytokine and antibody levels were analysed. Cytokine production wasanalysed using GLMM with a gamma distribution while all other data parameters were analysed using ANOVA.Infection reduced body-weight gain in ROH-HP mice to a smaller extent than in ROH-LP mice (HP 1.71 g v. LP 2.72 g, SED 1.5;P=0.035). In addition, ROH-HP mice had lower worm burdens than ROH-LP mice (P=0.077; Fig. 1). These effects were not seen inROL mice. Infection with H. bakeri increased levels of IL-13 (P=0.009) and IL-5 (P=0.001) in all mice. Across genotype, HP mice hadhigher levels of IL-5 (P=0.021) and lower levels of IL-6 (P=0.008) than LP-mice (Fig. 2). In ROL mice infection increased levels ofinterferon-g (IFN-g) (P=0.026) and decreased levels of IL-4 (P=0.003). Infection-increased IgG1 in both genetic lines but to a lesserextent in the ROL mice (P=0.027).Fig. 1. Worm burdens on LP and HP diet. Fig. 2. IL-5 and IL-6 on LP and HP diet.During H. bakeri infection, alongside a generalised increase in T-helper (Th) 2 cytokines (IL-5 and IL-13), selected immune responseswere found to be sensitive to protein nutrition (IL-5 and IL-6). It was also found that ROL mice produced a more inflammatory responseto infection, with increased levels of IL-6 and IFN-g compared with ROH mice. These observations suggest that narrow selection fordifferences in body weight may fundamentally alter host immune responses towards gastrointestinal parasites.1. Bu¨nger L, Laidlaw A, Bulfield G et al. (2001) Mamm Genome 12, 678–686.2. Coltherd JC, Bu¨nger L, Kyriazakis I et al. (2009) Parasitology 136, 1043–1055.3. Boulay M, Scott ME, Conly SL et al. (1998) Parasitology 116, 449–462.Proceedings of the Nutrition Society (2009), 68 (OCE), E101 doi:10.1017/S0029665109990577

Immune responses to macroparasites are sensitive to the interaction between genetic growth potential and protein nutrition in mice

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Coltherd, J.C., Babayan, S., Bünger, L., Kyriazakis, I., Allen, J.E., and 
Houdijk, J.G.M. (2009) Immune responses to macroparasites are sensitive 
to the interaction between genetic growth potential and protein nutrition in 
mice. Proceedings of the Nutrition Society, 68 (OCE3). E101. ISSN 0029-
665 
 
Copyright © 2009 Cambridge University Press 
 
A copy can be downloaded for personal non-commercial research or 
study, without prior permission or charge  
 
The content must not be changed in any way or reproduced in any format 
or medium without the formal permission of the copyright holder(s)  
 
When referring to this work, full bibliographic details must be given 
 
 
 
 
 
http://eprints.gla.ac.uk/81215/ 
 
 
 
 
 
 
Deposited on:  13 September 2013 
 
 
 
 
 
 
 
 
 
Enlighten – Research publications by members of the University of Glasgow 
http://eprints.gla.ac.uk 
Irish Section of The Nutrition Society, 17–19 June 2009
Immune responses to macroparasites are sensitive to the interaction
between genetic growth potential and protein nutrition in mice
J. C. Coltherd1, S. Babayan2, L. Bu¨nger3, I. Kyriazakis1,4, J. E. Allen2 and J. G. M. Houdijk1
1Animal Health, SAC, Edinburgh EH9 3JG, UK, 2IIIR, Ashworth Laboratories, Edinburgh EH9 3JT, UK,
3Animal Breeding and Genetics Team, SAC, Edinburgh EH9 3JG, UK and 4Veterinary Faculty, University of Thessaly,
43100 Karditsa, Greece
Animals selected narrowly for increased production traits may be penalised more from pathogen challenges than their unselected
counterparts. These genetic correlations between production and immune traits could be based on changes in the allocation of scarce
resources to immune functions. This possibility is addressed in mice that have been divergently selected over thirty-eight generations for high
(ROH) and low (ROL) body weight at 42 d of age(1). Infection with a gastrointestinal parasite in ROH mice results in a greater penalty
on resilience (body weight and food intake) and resistance (parasite egg numbers and worm burden) than in ROL mice(2). This penalty on
resilience is sensitive to protein nutrition, but the expected sensitivity of resistance to protein nutrition(3) is not significant. The aim of the
current study was to assess host immune responses that may underlie interactive effects of genetic potential and protein nutrition on resistance
to parasites.
In a 2 · 2 · 2 design, individually-housed male ROL and ROH mice were fed ad libitum diets with either 40 (LP) or 230 (HP) g crude
protein (N · 6.25)/kg and either sham infected or infected with Heligmosomoides bakeri larvae at 32 d of age (n 6). Feed intake and body
weight were assessed twice weekly for 28 d when worm burdens, cytokine and antibody levels were analysed. Cytokine production was
analysed using GLMM with a gamma distribution while all other data parameters were analysed using ANOVA.
Infection reduced body-weight gain in ROH-HP mice to a smaller extent than in ROH-LP mice (HP 1.71 g v. LP 2.72 g, SED 1.5;
P=0.035). In addition, ROH-HP mice had lower worm burdens than ROH-LP mice (P=0.077; Fig. 1). These effects were not seen in
ROL mice. Infection with H. bakeri increased levels of IL-13 (P=0.009) and IL-5 (P=0.001) in all mice. Across genotype, HP mice had
higher levels of IL-5 (P=0.021) and lower levels of IL-6 (P=0.008) than LP-mice (Fig. 2). In ROL mice infection increased levels of
interferon-g (IFN-g) (P=0.026) and decreased levels of IL-4 (P=0.003). Infection-increased IgG1 in both genetic lines but to a lesser
extent in the ROL mice (P=0.027).
Fig. 1. Worm burdens on LP and HP diet. Fig. 2. IL-5 and IL-6 on LP and HP diet.
During H. bakeri infection, alongside a generalised increase in T-helper (Th) 2 cytokines (IL-5 and IL-13), selected immune responses
were found to be sensitive to protein nutrition (IL-5 and IL-6). It was also found that ROL mice produced a more inflammatory response
to infection, with increased levels of IL-6 and IFN-g compared with ROH mice. These observations suggest that narrow selection for
differences in body weight may fundamentally alter host immune responses towards gastrointestinal parasites.
1. Bu¨nger L, Laidlaw A, Bulfield G et al. (2001) Mamm Genome 12, 678–686.
2. Coltherd JC, Bu¨nger L, Kyriazakis I et al. (2009) Parasitology 136, 1043–1055.
3. Boulay M, Scott ME, Conly SL et al. (1998) Parasitology 116, 449–462.
Proceedings of the Nutrition Society (2009), 68 (OCE), E101 doi:10.1017/S0029665109990577


Immune responses to macroparasites are sensitive to the interaction between genetic growth potential and protein nutrition in mice

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