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Published on: September 6, 2019
Formula-feeding is associated with shift towards Th1 cytokines
Beate Winkler1, Julia Aulenbach, Thomas Meyer
1Department of Paediatric Haematology/Oncology and Stem Cell Transplantation, University Children's Hospital, Joseph-Schneider-Str. 2, 97080, Würzburg, Germany.
Formula-feeding (FF) in infancy shifts immune responses toward Th1 cytokines, impacting T-cell differentiation and cytokine profiles throughout childhood. This early feeding choice influences immune maturation and may affect later autoimmune disease development.
Area of Science:
- Immunology
- Pediatrics
- Nutrition
Background:
- Early life nutrition, specifically breast-feeding (BF) versus formula-feeding (FF), is hypothesized to influence immune system development.
- T-cell subsets and cytokine production are critical components of immune maturation during infancy and childhood.
Purpose of the Study:
- To investigate the impact of BF versus FF on T-cell subpopulations and cytokine production in infants and children.
- To analyze serum cytokine levels and the Th1/Th2 balance in relation to early feeding practices.
Main Methods:
- Blood samples from 191 healthy infants and children were analyzed.
- T-cell subsets and intracellular cytokines (IFNγ, IL4) were determined by flow cytometry after in vitro stimulation.
- Serum concentrations of IFNγ and IL4 were measured via ELISA, and an IFNγ/IL4 ratio was calculated.
Main Results:
- Formula-fed children exhibited higher numbers of memory T and T helper cells compared to breast-fed infants.
- Increased IFNγ-positive memory T-cells were observed in formula-fed children up to age 6.
- Formula-fed children showed elevated serum IFNγ levels and an increased IFNγ/IL4 ratio, indicating a shift towards Th1 responses.
Conclusions:
- Early feeding practices significantly influence immune system maturation and cytokine profiles throughout childhood.
- Formula-feeding induces a Th1-biased immune response in children, which persists even after cessation of BF.
- This Th1 shift may have long-term implications for the development of autoimmune diseases later in life.
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