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Low Interleukin 10 Production at Birth Is a Risk Factor for Atopic Dermatitis in Neonates with Bifidobacterium
Shuichi Suzuki1,2, Eduardo Campos-Alberto3, Yoshinori Morita3
1Department of Pediatrics, Graduate School of Medicine, Chiba University, Chiba, Japanseeyou@msj.biglobe.ne.jp.
Insights
Infants with lower interleukin-10 (IL-10) at birth show higher atopic dermatitis (AD) risk. Early gut bacteria colonization doesn't fully offset this risk, suggesting impaired IL-10 response is key.
Area of Science:
- Immunology
- Microbiology
- Pediatrics
Background:
- Early life immune dysregulation and gut microbiota alterations are implicated in allergic disease development, such as atopic dermatitis (AD).
- Simultaneous investigation of neonatal immune responses to microbes and gut bacterial colonization is limited.
Purpose of the Study:
- To analyze neonatal immune responses to microbial stimuli and beneficial gut bacteria colonization.
- To determine the relationship between these factors and the development of AD in a birth cohort.
Main Methods:
- Recruited pregnant women and followed infants until 7 months.
- Measured interleukin-10 (IL-10) from cord blood mononuclear cells (CBMCs) stimulated with specific bacteria and bacterial components.
- Quantified fecal Bifidobacterium counts and assessed AD development via questionnaire.
Main Results:
- Infants who developed AD exhibited significantly lower IL-10 levels in response to all microbial stimuli compared to healthy infants.
- In infants with Bifidobacterium colonization, higher IL-10 release was inversely associated with AD incidence.
Conclusions:
- Impaired IL-10 production in neonates may increase the risk of developing infantile atopic dermatitis.
- This risk persists even in the presence of early intestinal Bifidobacterium colonization.
Background:
Altered regulatory immune responses to microbial stimuli and intestinal colonization of beneficial bacteria early in life may contribute to the development of allergic diseases (e.g., atopic dermatitis [AD]). However, few reports have investigated these factors simultaneously. The purpose of this study was to analyze neonatal immune responses to microbial stimuli as well as intestinal colonization of beneficial bacteria, in relation to the development of AD in a birth cohort.
Methods:
Pregnant women were recruited, and their infants were followed up until 7 months of age. Levels of interleukin (IL)-10 released from cord-blood mononuclear cells (CBMCs) stimulated with heat-killed gram-positive bacteria (Bifidobacterium bifidum and Lactobacillus rhamnosus GG) and Lactobacillus-derived peptidoglycan were measured. Fecal Bifidobacterium counts at 4 days and 1 month were quantified using real-time polymerase chain reaction. The development of AD was determined by means of a questionnaire at 7 months of age.
Results:
The levels of released IL-10 were significantly lower in infants with AD (n = 17) than in infants without AD (n = 53) for all stimuli. In infants with fecal Bifidobacterium, the incidence of AD was inversely associated with the release of IL-10 from cord blood mononuclear cells.
Conclusion:
Our findings suggest that impaired IL-10 production in response to microbial stimuli at birth may be associated with an increased risk of developing infantile AD, even in infants with early colonization of intestinal bifidobacteria.
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