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In vivo dysfunction of the term alveolar macrophage after in utero ethanol exposure
- Source :
- Alcoholism, clinical and experimental research. 31(2)
- Publication Year :
- 2007
-
Abstract
- Background: The effects of in utero alcohol exposure on the immune function of the newborn remain under investigation. Fetal ethanol (ETOH) exposure increases oxidative stress in the developing lung, in part due to decreased availability of the antioxidant glutathione (GSH). We have previously shown that in utero ETOH impairs alveolar macrophage phagocytosis and viability in the premature pup, while maintaining GSH availability with maternal supplementation of S-adenosyl-methionine (SAM) during ETOH ingestion improves macrophage function and viability. We hypothesized that dysfunction of the neonatal alveolar macrophage exposed to ETOH in utero would persist at term gestation. Methods: Using a guinea-pig model of fetal ETOH exposure, timed-pregnant guinea-pigs were pair-fed ETOH±the GSH precursor SAM and the diet continued until spontaneous delivery. Term alveolar macrophages were evaluated using fluorescent microscopy for phagocytosis and apoptosis after in vitro incubation with Staphalococcus aureus. Using an in vivo model of intranasal Staph. aureus inoculation, the in vivo function of the term alveolar macrophage was also investigated using confocal fluorescent analysis. Results: In utero ETOH exposure increased oxidant stress in the alveolar macrophage and decreased phagocytosis and viability in vitro and in vivo. Confocal analysis of phagocytosis in vivo demonstrated a marked impairment of internalization of the bacteria by the ETOH-exposed alveolar macrophage. The addition of SAM during maternal ETOH ingestion prevented loss of alveolar macrophage function and viability in vitro and in vivo. Conclusions: In utero ETOH exposure impairs alveolar macrophage function and viability in vitro and in vivo even at term gestation. The ETOH-induced changes in macrophage function and viability can be ablated with maternal SAM supplementation. Further investigations are required to identify the mechanisms of ETOH-induced derangement of phagocytosis in the neonatal alveolar macrophage and the clinical ramifications of altered immune function after in utero alcohol exposure for the newborn.
- Subjects :
- endocrine system
Staphylococcus aureus
Cell Survival
Phagocytosis
Guinea Pigs
Medicine (miscellaneous)
Apoptosis
Biology
Toxicology
medicine.disease_cause
Andrology
chemistry.chemical_compound
In vivo
Pregnancy
mental disorders
Macrophages, Alveolar
medicine
Macrophage
Animals
reproductive and urinary physiology
Lung
Ethanol
Central Nervous System Depressants
Glutathione
Psychiatry and Mental health
Oxidative Stress
medicine.anatomical_structure
chemistry
Animals, Newborn
In utero
Maternal Exposure
Prenatal Exposure Delayed Effects
Immunology
Alveolar macrophage
Female
Oxidative stress
Subjects
Details
- ISSN :
- 01456008
- Volume :
- 31
- Issue :
- 2
- Database :
- OpenAIRE
- Journal :
- Alcoholism, clinical and experimental research
- Accession number :
- edsair.doi.dedup.....fe626cc97c0bf489b41266d5ef63f5b4