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Published on: July 13, 2014
In utero ethanol exposure impairs defenses against experimental group B streptococcus in the term Guinea pig lung
Theresa W Gauthier1, Paula A Young, Levan Gabelaia
1Department of Pediatrics, Division of Neonatal-Perinatal Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
Insights
Fetal alcohol exposure weakens newborn lung immunity, increasing infection risk. Supplementing with S-adenosyl-methionine or glutathione protects against bacterial pneumonia in infants exposed to alcohol in utero.
Area of Science:
- Neonatal immunology
- Pulmonary medicine
- Toxicology
Background:
- Fetal alcohol exposure's impact on neonatal lung injury and infection risk is under investigation.
- Alveolar macrophages (AM) are crucial for lung immune defense.
- In utero ethanol (ETOH) exposure impairs AM function in guinea pigs.
Purpose of the Study:
- To investigate if fetal ETOH exposure increases the risk of pulmonary infection in vivo.
- To evaluate the protective effects of S-adenosyl-methionine (SAM-e) and glutathione (GSH) against ETOH-induced lung injury.
Main Methods:
- A guinea pig model of fetal ETOH exposure and group B Streptococcus (GBS) pneumonia was developed.
- Pregnant guinea pigs received ETOH +/- SAM-e supplementation.
- Neonatal pups were challenged with GBS, with some receiving inhaled GSH pretreatment.
Main Results:
- ETOH-exposed pups showed increased lung infection and sepsis, with deficient AM phagocytosis of GBS.
- SAM-e supplementation attenuated infection and improved AM phagocytosis in ETOH-exposed pups.
- Inhaled GSH therapy protected ETOH-exposed pups from GBS infection.
Conclusions:
- In utero ETOH exposure compromises neonatal lung defense against bacterial infection.
- Maintaining glutathione availability protects the ETOH-exposed neonatal lung.
- Exogenous GSH may therapeutically augment neonatal AM function.
Background:
The effects of fetal alcohol exposure on the risks of neonatal lung injury and infection remain under investigation. The resident alveolar macrophage (AM) is the first line of immune defense against pulmonary infections. In utero ethanol (ETOH) exposure deranges the function of both premature and term guinea pig AM. We hypothesized that fetal ETOH exposure would increase the risk of pulmonary infection in vivo.
Methods:
We developed a novel in vivo model of group B Streptococcus (GBS) pneumonia using our established guinea pig model of fetal ETOH exposure. Timed-pregnant guinea pigs were pair fed +/-ETOH and some were supplemented with the glutathione (GSH) precursor S-adenosyl-methionine (SAM-e). Term pups were given GBS intratracheally while some were pretreated with inhaled GSH prior to the experimental GBS. Neonatal lung and whole blood were evaluated for GBS while isolated AM were evaluated using fluorescent microscopy for GBS phagocytosis.
Results:
Ethanol-exposed pups demonstrated increased lung infection and sepsis while AM phagocytosis of GBS was deficient compared with control. When SAM-e was added to the maternal diet containing ETOH, neonatal lung and systemic infection from GBS was attenuated and AM phagocytosis was improved. Inhaled GSH therapy prior to GBS similarly protected the ETOH-exposed pup from lung and systemic infection.
Conclusions:
In utero ETOH exposure impaired the neonatal lung's defense against experimental GBS, while maintaining GSH availability protected the ETOH-exposed lung. This study suggested that fetal alcohol exposure deranges the neonatal lung's defense against bacterial infection, and support further investigations into the potential therapeutic role for exogenous GSH to augment neonatal AM function.
