Abstract
Bifidobacterium breve M-16V is a probiotic bacterial strain with efficacy in infants achieved by suppressing T-helper type (Th) 2 immune responses and modulating the systemic Th1/Th2 balance. Exposure to air pollution during pregnancy increases asthma susceptibility in offspring. The aim of this study was to investigate the effects of the maternal intake of B. breve M-16V on susceptibility to asthma accelerated by prenatal exposure to air pollution. The intake of B. breve M-16V in residual oil fly ash (ROFA)-exposed pregnant mice resulted in fewer eosinophils in the bronchoalveolar lavage fluid of neonatal mice and reduced allergic lung inflammation. The expressions of Th2 cytokines including IL-5 and IL-13 were decreased in neonatal mice from ROFA-exposed mothers fed B. breve M-16V. The analysis of fecal microbiota from neonatal mice revealed that the intake of B. breve M-16V by mothers changed the composition of fecal microbiota in neonatal mice, which resulted in a decreased population of Firmicutes. Moreover, several bacterial strains of fecal microbiota from neonatal mice had a strong correlation with Th2 cytokines and histological score. These results suggest that the maternal intake of M-16V might have beneficial effects in neonates by preventing and/or alleviating allergic reactions accelerated by prenatal exposure to air pollution.
Highlights
The increasing incidence of asthma in early life suggests that prenatal environmental exposure may influence susceptibility to allergic airway diseases [1,2,3]
As shown in S1 Fig, there were no significant differences in mucin score or allergic Th2 gene expressions including IL-4, IL-5, IL-13, and Muc5ac between control (AIN-93G) and M-16V diet mice not exposed to residual oil fly ash (ROFA)
We confirmed that ROFA exposure of mothers on the control diet aggravated the response of their neonatal mice as assessed by mucin score and gene expressions of IL-5 and IL-13 (S2 Fig)
Summary
The aim of this study was to investigate the effects of the maternal intake of B. breve M-16V on susceptibility to asthma accelerated by prenatal exposure to air pollution
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