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30.06.2017 | Original Contribution | Ausgabe 6/2018

European Journal of Nutrition 6/2018

The dietary form of choline during lactation affects maternal immune function in rats

European Journal of Nutrition > Ausgabe 6/2018
N. S. Dellschaft, C. Richard, E. D. Lewis, S. Goruk, R. L. Jacobs, J. M. Curtis, C. J. Field
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1007/​s00394-017-1493-0) contains supplementary material, which is available to authorized users.



The present study was designed to determine the effects of both choline form and availability on maternal immune function during lactation.


Sprague–Dawley rats were randomized to one of the three diets 24–48 h before parturition and fed ad libitum until 21 days postnatal: 1 g/kg choline as free choline (C, n = 11), the current form, and amount of choline in commercial diets; 1 g/kg choline as phosphatidylcholine (PC1, n = 11); or 2.5 g/kg choline as PC (PC2.5, n = 8). Choline metabolites in offspring stomach contents were quantified. At 21 days, lymphocytes from mothers’ mesenteric lymph nodes and spleens were isolated and phenotypes and ex vivo cytokine production after mitogen exposure were determined.


There was a higher proportion of choline and a lower proportion of lyso-PC in stomach contents (representing dam’s milk) of C pups compared to PC1. In the mesenteric lymph nodes, feeding PC1 compared to C led to a higher IL-2 production after Concanavalin A (ConA) stimulation and a higher proportion of T cells (CD3+) and a lower proportion of B cells [immunoglobulin (Ig)κ, CD45RA+, and IgM+; P < 0.05]. Splenocytes from the PC1 group produced more IL-6 and TNF-α after lipopolysaccharides stimulation compared to C (P < 0.05). Splenocytes from the PC2.5 group produced more IL-2 and IL-6 after ConA stimulation compared to PC1 (P < 0.05).


Feeding choline as PC in the maternal diet improved the ability of immune cells to respond ex vivo to mitogens and increasing the amount of PC in the diet further improved T cell proliferation.

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