Hostname: page-component-cd9895bd7-fscjk Total loading time: 0 Render date: 2024-12-22T15:05:55.592Z Has data issue: false hasContentIssue false

Rapid restoration of immunity to parasites in lactating rats by changing nutrient demand

Published online by Cambridge University Press:  19 November 2010

P. Sakkas
Affiliation:
Animal Health, SAC, Edinburgh EH9 3JG, UK
L. A. Jones
Affiliation:
Animal Health, SAC, Edinburgh EH9 3JG, UK
J. G. M. Houdijk
Affiliation:
Animal Health, SAC, Edinburgh EH9 3JG, UK
D. P. Knox
Affiliation:
Parasitology Division, Moredun Research Institute, Penicuik EH26 0PZ, UK
I. Kyriazakis
Affiliation:
Animal Health, SAC, Edinburgh EH9 3JG, UK Veterinary Faculty, University of Thessaly, 43100 Karditsa, Greece
Rights & Permissions [Opens in a new window]

Abstract

Type
Abstract
Copyright
Copyright © The Authors 2010

The periparturient relaxation of immunity to parasites in mammals may have a nutritional basis(Reference Coop and Kyriazakis1). Indeed, at times of protein scarcity, resistance and immunity to the intestinal parasite Nippostrongylus brasiliensis in lactating rats improves with increased protein supply(Reference Jones, Houdijk and Knox2) and reduced litter size and thus reduced nutrient demand(Reference Normanton, Houdijk and Jessop3). Here, we use the latter observation to assess the rate at which improved host nutritional status can improve periparturient resistance and immunity.

Second parity rats were infected with 1600 N. brasiliensis larvae prior to mating (primary infection). Upon parturition (d0), dams were fed ad libitum a low-protein food (100 g CP/kg DM) and were either nursing 12 pups (LS12) or 3 pups (LS3) throughout, or nursed 12 pups until day 5 when their litter was adjusted to 3 pups (LS12-3). Rats were re-infected with 1600 larvae on d2 (secondary infection). Food intake, and dam and litter weight were assessed daily until either d5 (for LS12 only), or d8 and d11 (all treatments) when the number of worms, worm eggs in the colon contents (EIC) and small intestinal mucosal inflammatory cells per villus-crypt unit (vcu) were assessed. These data were log-transformed prior to statistical analysis through ANOVA.

Fig. 1. Dam weight.

Fig. 2. Eggs in colon.

Fig. 3. Mucosal mast cells.

Litter size manipulation did not affect feed intake (data not shown). Figure 1 shows that the body weight of LS12 dams gradually reduced, while that of LS12-3 dams gradually increased to that of LS3 dams. Sampling time post challenge did not interact with litter size manipulation for any of the parasitological and immunological parameters (P>0.10). However, averaged over sampling points, LS12-3 and LS3 dams had fewer EIC (Fig. 2; P<0.001), more mucosal mast cells (Fig. 3; P<0.01) and worm burdens (P<0.05; data not shown) than LS12 dams. Litter size manipulation did not affect the number of eosinophils or goblet cells (P>0.10; data not shown).

These results confirm that the resistance to N. brasiliensis is sensitive to nutrient demand(Reference Normanton, Houdijk and Jessop3). The cessation of body weight loss following pup removal suggests that nutrient supply changed from scarce to more than adequate. Since worm burdens and mucosal mast cell numbers taken 3 d following pup removal were similar to those in dams rearing small litters throughout, our results support the view that nutrient supplementation can rapidly improve periparturient resistance and immunity to parasites.

References

1.Coop, RL & Kyriazakis, I (1999) Nutrition–parasite interaction. Vet Parasitol 84, 187204.CrossRefGoogle ScholarPubMed
2.Jones, LA, Houdijk, JGM, Knox, DP et al. (2009) Immunomodulatory effects of dietary protein during Nippostrongylus brasiliensis infection in lactating rats. Parasite Immunol 31, 412421.CrossRefGoogle ScholarPubMed
3.Normanton, H, Houdijk, JGM, Jessop, NS et al. (2007) The effects of changes in nutritional demand on gastrointestinal parasitism in lactating rats. Br J Nutr 97, 104110.CrossRefGoogle ScholarPubMed
Figure 0

Fig. 1. Dam weight.

Figure 1

Fig. 2. Eggs in colon.

Figure 2

Fig. 3. Mucosal mast cells.