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Published on: March 25, 2016
Maternal aspartame exposure alters lung Th1/Th2 cytokine balance in offspring through nuclear factor-κB activation
Hsiao-Chi Chuang1, Yu-Chen S H Yang2, Hsiu-Chu Chou3
1School of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Insights
Maternal aspartame intake during pregnancy and lactation may impact offspring lung health by altering immune responses. This study found it skewed the Th1/Th2 cytokine balance and activated nuclear factor-κB in offspring lungs.
Area of Science:
- Immunology
- Toxicology
- Microbiome Research
Background:
- Epidemiological studies link maternal nonnutritive sweetener intake to childhood asthma.
- Aspartame is a common nonnutritive sweetener with potential health implications.
Purpose of the Study:
- To investigate the effects of maternal aspartame exposure on offspring lung immune balance.
- To explore the role of intestinal microbiota and nuclear factor-κB (NF-κB) activation in mediating these effects.
Main Methods:
- Pregnant mice received either water or aspartame-supplemented water during pregnancy and lactation.
- Offspring lung tissues and gut microbiota were analyzed for immune markers and microbial composition.
- Immunoglobulin E (IgE) levels and cytokine profiles (Th1/Th2) were measured.
Main Results:
- Maternal aspartame exposure increased offspring body weight and elevated Th2 cytokines (IL-4, IL-5, IL-13), IL-17, and IgE.
- A decrease in the Th1 cytokine interferon-gamma (IFN-γ) was observed, indicating an altered Th1/Th2 balance.
- Increased nuclear factor-κB (NF-κB) activation was noted in offspring lungs, while gut microbiota composition remained unchanged.
Conclusions:
- Maternal aspartame exposure influences the lung Th1/Th2 cytokine balance in offspring.
- Nuclear factor-κB (NF-κB) activation appears to be a key mechanism mediating these immune alterations.
Background:
Epidemiological evidence suggests that maternal intake of nonnutritive sweeteners is positively associated with early childhood asthma incidence. We investigated the effects of maternal aspartame exposure during pregnancy and lactation on lung Th1/Th2 cytokine balance and intestinal microbiota in offspring and explored the mechanisms that mediate these effects.
Method:
Pregnant BALB/c mice were randomly divided on gestational day 7 into two dietary intervention groups: control (drinking water only) and aspartame (drinking water +0.25 g/L aspartame) groups. The dams nursed their offspring for 3 weeks. On postnatal day 21, heart blood samples were collected, and immunoglobulin E levels were measured. Microorganisms from the lower gastrointestinal tract were sampled using a culture-independent approach. Lung tissues were harvested for biochemical analyses.
Results:
Maternal aspartame exposure increased the body weight of the dams from gestational day 7 to postnatal day 21 and the body weight of the offspring from birth to postnatal day 21. Maternal aspartame exposure significantly increased the levels of Th2 cytokines (interleukin [IL]-4, IL-5, and IL-13) and IL-17 and immunoglobulin E but reduced that of a Th1 cytokine (interferon-γ) in the offspring's lung tissues. The altered Th1/Th2 balance was accompanied by increased lung nuclear factor-κB activation. The bacterial composition and alpha-diversity of the gut microbiota of the offspring did not differ significantly between the control and aspartame groups.
Conclusion:
Our findings suggest maternal aspartame exposure influences lung Th1/Th2 cytokine balance in offspring through nuclear factor-κB activation.
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