Cited by 61Prenatal Substance Exposure EffectsNeonatal Respiratory Health ResearchAlcohol Consumption and Health Effects

Fetal Alcohol Exposure Impairs Alveolar Macrophage Function via Decreased Glutathione Availability

Gauthier, Theresa W, Ping, Xiao-Du, Harris, Frank L, Wong, Michael, Elbahesh, Husni, Brown, Lou Ann S·2005·Pediatric Research

Abstract

Immature function of the alveolar macrophage increases the risk of pulmonary infections in premature newborns. In utero alcohol increases fetal systemic oxidative stress. Because the premature lung is deficient in glutathione (GSH), we hypothesized that chronic in utero alcohol (ethanol) exposure exacerbates the oxidative stress within the developing lung, thereby impairing alveolar macrophage function. Additionally, we evaluated the effects of in vivo and in vitro GSH availability on ethanol-exposed macrophage function. Using a guinea pig model of chronic in utero ethanol exposure, fetal epithelial lining fluid (ELF) and alveolar macrophage GSH were decreased with increased markers of oxidative stress. Ethanol-exposed macrophage exhibited impaired phagocytosis and increased apoptosis compared with gestational control. When the GSH precursor S-adenosyl-methionine (SAM) was added to the maternal drinking water containing ethanol, fetal ELF and macrophage GSH were maintained and ELF oxidative stress diminished. In vivo maternal SAM therapy maintained macrophage phagocytosis and decreased apoptosis. In vitro GSH supplements also improved phagocytosis and viability in both premature and ethanol-exposed macrophage. This suggested that in utero ethanol impaired premature macrophage function and viability via decreased GSH availability. Furthermore, GSH supplementation during and after ethanol exposure improved fetal macrophage function and viability. These results add a new dimension to the detrimental effects of fetal alcohol exposure on the developing alveolar macrophage, raising the possibility of GSH therapy to augment premature alveolar macrophage function.

Integrity signals

Registry

Crossref · 10.1203/01.pdr.0000149108.44152.d3

Cites

56 of 56 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Chronic and/or excessive alcohol intake can cause ARDS and other types of pulmonary dysfunction characterized by reduced air exchange rates with increased lung epithelial barrier dysfunction, possibly through increased oxidative stress and MDA and 4-HNE adducts.

    “Chronic and/or excessive alcohol intake can cause acute respiratory distress syndrome (ARDS) and other types of pulmonary dysfunction characterized by reduced air exchange rates with increased lung epithelial barrier dysfunction, possibly through increased oxidative stress and MDA and 4-HNE adducts164,234.”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Gauthier, T. W., Ping, X.-D., Harris, F. L., Wong, M., Elbahesh, H., & Brown, L. A. S.
Affiliations
Emory University (US)
Corresponding author
Gauthier, Theresa W
Venue
Pediatric Research
Published
2005-01
Volume
57
Issue
1
Pages
76-81
ISSN
  • 0031-3998 (ISSN-L)
  • 1530-0447
OpenAlex
W2066072238
Cited by
61
References
56
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 2 · 2018: 1 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 6
FWCI
1.77
Type
journal article
Language
en
Open access
closed
Locations
  • Pediatric Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r03hd039651-02)
  • National Institute on Alcohol Abuse and Alcoholism (R01AA013979)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD39651)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
Keywords
prenatal alcohol exposure, ethanol, alveolar macrophages, glutathione, oxidative stress, epithelial lining fluid, phagocytosis, macrophage apoptosis, S-adenosylmethionine, glutathione supplementation
MeSH terms
Alcohol Drinking, Ethanol, Animals, Cell Survival, Central Nervous System Depressants, Disease Models, Animal, Epithelium, Female, Glutathione, Guinea Pigs, Macrophages, Phagocytosis, S-Adenosylmethionine, Time Factors, Lipid Peroxidation, Apoptosis, Oxidative Stress, Maternal Exposure, In Situ Nick-End Labeling

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review