Electroacupuncture may protect pulmonary dysplasia in offspring with perinatal nicotine exposure by altering maternal gut microbiota and metabolites.
Publication Year:
2024
PubMed ID:
39850138
Funding Grants:
Public Summary:
Every year, thousands of babies are born with underdeveloped lungs due to harmful exposures during pregnancy—one of the most common being nicotine. This can lead to lifelong breathing problems and even affect future generations. But what if we could use the body’s own biology—and even stem cell–based strategies—to protect developing lungs?
This study explores how a traditional therapy, electroacupuncture (EA), may help counteract the damaging effects of nicotine exposure during pregnancy. The researchers focused on how EA influences the mother’s gut microbiome—the community of bacteria in the digestive system—and how this, in turn, affects the baby’s lung development.
The gut microbiome produces short-chain fatty acids (SCFAs), natural compounds that help regulate inflammation and tissue development. These SCFAs can influence how organs like the lungs grow and repair themselves—an area of great interest to stem cell researchers working to regenerate damaged tissues.
In this study, pregnant rats exposed to nicotine showed disrupted gut bacteria and lower SCFA levels. Their offspring had poor lung development and function. But when the mothers received EA treatment, their gut microbiomes improved, SCFA levels increased, and their babies’ lungs developed more normally.
To test whether the gut bacteria were truly responsible, the researchers used antibiotics to wipe out the microbiome. Without these bacteria, EA no longer helped the babies’ lungs—confirming the critical role of the gut-lung connection.
This study highlights how biological systems—like the gut microbiome—can be harnessed to support organ development and repair. It also opens the door to future therapies that combine stem cell–based approaches with microbiome modulation to treat or prevent lung diseases in newborns.
By connecting ancient practices like acupuncture with cutting-edge science in stem cells and regenerative medicine, this research offers new hope for protecting the most vulnerable lungs—before a baby even takes its first breath.
Scientific Abstract:
BACKGROUND: Perinatal nicotine exposure (PNE) induces pulmonary dysplasia in offspring and it increases the risk of respiratory diseases both in offspring and across generations. The maternal gut microbiota and its metabolites, such as short-chain fatty acids (SCFAs), can regulate fetal lung development and are susceptible to nicotine exposure. Therefore, modulation of PNE-induced changes in maternal gut microbiota and SCFAs may prevent the occurrence of pulmonary dysplasia in offspring. OBJECTIVE: Our previous studies demonstrated that electroacupuncture (EA) ameliorated PNE-induced impairment in offspring lung development. To further our study, we aimed to determine whether the protective effect of EA is associated with the modulation of changes in maternal gut microbiota and SCFAs. METHODS: We observed changes in maternal gut microbiota and serum SCFA levels in both mother and offspring after EA treatment using a PNE rat model. Furthermore, using broad-spectrum antibiotics, we established a pseudo-germ-free PNE rat model to explore whether EA can protect offspring's pulmonary function and lung morphology in the presence of depleted maternal gut microbiota. RESULTS: Our study revealed that EA increased the community richness (Sobs index) of perinatal nicotine-exposed maternal gut microbiota and the abundance of beneficial bacteria (RF39, Clostridia, Oscillospirales, etc.). This was accompanied by an upregulated serum levels of acetate, butyrate, and total SCFAs in both mother and offspring rats, as well as stimulated expression of SCFA receptors (GPR41 and GPR43) in the lung tissue of offspring rats. However, the beneficial effects of EA on offspring pulmonary function (FVC, PEF, PIF, and Cdyn) and lung morphology (alveolar number and MLI) were lost after maternal gut microbiota depletion. CONCLUSION: These findings suggest that EA may exert its therapeutic effects on PNE-induced lung phenotype by altering maternal gut microbiota. The likely mechanism involves the associated improvement in serum SCFA levels in both mother and offspring, as well as the upregulation of SCFA receptors in the lung tissue of offspring.
