Lower proportion of CD45R0(+) cells and deficient interleukin-10 production by formula-fed infants, compared with human-fed, is corrected with supplementation of long-chain polyunsaturated fatty acids

Background: The immune consequences of adding 20:4n-6 and 22:6n-3 fatty aci ds to preterm infant formula are not known. Methods: The effect of feeding preterm infants (14-42 days of age) human mi lk (Human Milk group), infant formula formula group), or formula with added long-chain polyunsaturated fatty acids 20:4n-6 and 22:6n-3 (Formula + LCP group) on isolated peripheral blood lymphocytes (by flow cytometry) and lip id composition (by gas-liquid chromatography) was determined. Lymphocytes w ere stimulated in vitro with phytohemagglutinin to measure soluble interleu kin (sIL)-2R and IL-10 production (by enzyme-linked immunosorbent assay). Results: With age, the percentage of CD3(+)CD4(+) T cells and the percentag e of CD20(+) cells increased in the Human Milk and Formula + LCP groups (P < 0.05), but not in the unsupplemented Formula group. Compared with the For mula group, CD4(+) cells from the Formula + LCP and Human Milk groups expre ssed more CD45R0 (antigen mature) and less CD45RA (antigen naive) at 42 day s of age (P < 0.05). At 42 days, IL-10 production was lower (P < 0.05) in c ells of the Formula group than in cells of the Human Milk group. Production of IL-10 by the cells of the Formula + LCP group was not different from th at produced by the Human Milk group cells. An age-related decrease (P < 0.0 5) in sIL-2R production by Formula + LCP lymphocytes was observed, but sIL- 2R production at 42 days in the Formula + LCP group did not differ signific antly from that in the Human Milk group. Compared with Formula alone, addin g LCP to formula resulted in a lower C18:2n-6 and higher C20:4n-6 content i n lymphocyte phospholipids (P < 0.05). Conclusions: Adding LCP to a preterm infant formula resulted in lymphocyte populations, phospholipid composition, cytokine production, and antigen mat urity that are more consistent with that in human milk-fed infants. This ma y affect the ability of the infant to respond to immune challenges.