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Arachidonic acid‐ and docosahexaenoic acid‐enriched formulas modulate antigen‐specific T cell responses against influenza virus in neonatal piglets
Author(s) -
BassaganyaRiera Josep,
Guri Amir J,
Noble Alexis M,
Reynolds Kathryn A,
King Jennifer,
Wood Cinthia M,
Ashby Michael,
Rai Deshanie,
Hontecillas Raquel
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a377
Subject(s) - docosahexaenoic acid , immune system , arachidonic acid , antigen , virus , infant formula , weaning , immunology , biology , influenza a virus , cd8 , medicine , virology , fatty acid , polyunsaturated fatty acid , endocrinology , biochemistry , enzyme
While the immunomodulatory effects of feeding either arachidonic acid (AA) or docosahexaenoic acid (DHA) separately have been previously investigated, little is known about their immunomodulatory efficacy when fed in combination as infant formula ingredients. This study investigates the ability of AA/DHA‐enriched infant formula to modulate immune responses in the neonate in response to an inactivated influenza virus vaccine. Neonatal piglets (n=48) were weaned on day 2 of age and distributed into 16 blocks of 3 littermate piglets each. Within each block, piglets were randomly assigned to a control formula, AA/DHA‐enriched formula (0.63% AA and 0.34% DHA) or sow's milk for 30 days. On d 9, 8 blocks of piglets were immunized with an inactivated influenza virus vaccine. On days 0, 9, 16, 23 and 30 post‐weaning we measured influenza virus‐specific proliferation. Dietary AA/DHA‐supplementation and sow's milk modulated influenza virus‐specific CD4 + and CD8 + T cell ex vivo lymphoproliferative responses on d 23 post‐immunization in comparison to the unsupplemented control formula. The immunomodulatory effects of AA/DHA‐enriched formulas were consistent with upregulation of interleukin‐10 (IL‐10) in PBMC. Overall, the AA/DHA‐enriched formula modulated antigen‐specific T cell responses through an IL‐10‐dependent mechanism.