Formula-feeding is associated with shift towards Th1 cytokines

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• 作者：Beate Winkler ; Julia Aulenbach ; Thomas Meyer…
• 关键词：Breast ; feeding ; Cytokines ; Th1/Th2 ; Flow cytometry
• 刊名：European Journal of Nutrition
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：54
• 期：1
• 页码：129-138
• 全文大小：445 KB
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• 刊物类别：Chemistry and Materials Science
• 刊物主题：Chemistry
  Nutrition
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1436-6215

文摘

Purpose Breast-feeding (BF) versus formula-feeding (FF) may be a factor for the development and differentiation of T-cell subsets and cytokine production in infancy and childhood. We therefore investigated T-cell subpopulations and their cytokine production by flow cytometry as well as cytokine levels in serum samples in breast-fed versus formula-fed infants and children. Methods Heparinised blood was taken from 191 healthy infants and children. Peripheral blood mononuclear cells were stimulated with phorbol-mystriate-acetate and ionomycin in the presence of brefeldin. T-cell subsets and cytokines were determined by flow cytometry. Furthermore, serum concentrations of IFNγ and IL4 were measured using ELISA. An IFNγ/IL4 ratio was calculated to estimate the Th1/Th2 balance. Results Children who were formula-fed show higher numbers of memory T and T helper cells. After stimulation, the number of IFNγ-positive memory T-cells was increased up to the age of 6?years. Breast-fed infants show higher percentages of IL4-positive T helper cells. At ELISA determination, formula-fed children showed higher IFNγ levels than breast-fed children, while IL4 levels did not differ. The IFNγ/IL4 ratio (FACS and ELISA) was elevated in formula-fed infants and children. Conclusion This systematic analysis of cytokine profiles during childhood in dependency of BF allows a better understanding of immune maturation and demonstrates the influence of early feeding on immune function throughout childhood, even after cessation of BF. FF induces a shift towards Th1 cytokines in children. This may have an influence on the development of autoimmune disease in later life.