The Ontogeny of Pulmonary Defenses: Alveolar Macrophage Function in Neonatal and Juvenile Rhesus Monkeys

Kurland, Geoffrey; Cheung, Anthony; Miller, Michael E.; Ayin, Susan A.; Cho, Maung M; Ford, Elizabeth W.

doi:10.1203/00006450-198803000-00013

Cited by 63 publications

(33 citation statements)

References 29 publications

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“…As predicted by previous studies on AM number after birth (13,17,19), there was an exponential increase in the number of AM during the first postnatal week with a linear increase thereafter to adult levels (Fig. 1).…”

Section: Resultssupporting

confidence: 65%

“…Through the prior work of several investigators (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24), it is known that an influx of AM into the rabbit lung precedes birth by 24 h. This is followed by an exponential increase in AM number during the first week after delivery. During postnatal lung development, there is a gradual shift from a homogeneous, monocyte-like population to a more heterogeneous population of AM of varying density and function (14,(25)(26)(27)(28)(29)(30).…”

mentioning

confidence: 99%

“…During postnatal lung development, there is a gradual shift from a homogeneous, monocyte-like population to a more heterogeneous population of AM of varying density and function (14,(25)(26)(27)(28)(29)(30). Although the ultrastructure and certain biologic functions of AM isolated from postnatal rabbits have been defined (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25), there is scarce information about AM growth factor production and what effect such cytokines may have on lung parenchymal differentiation during postnatal development. It is unknown when AM become functionally capable of TGFa secretion during postnatal development and if this capability extends to (9)(10)(11)(12)(13).…”

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confidence: 99%

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Secretion of Transforming Growth Factor-α (TGFα) by Postnatal Rabbit Alveolar Macrophages

et al. 1995

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Section: Resultssupporting

confidence: 65%

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confidence: 99%

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confidence: 99%

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Secretion of Transforming Growth Factor-α (TGFα) by Postnatal Rabbit Alveolar Macrophages

et al. 1995

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“…The antimicrobial functions of AM include phagocytosis, oxidant mediated microbial killing, and the recruitment of leukocytes by pro-inflammatory cytokines. Studies in the rhesus monkey have suggested that AM in the neonatal lung are deficient in a range of antimicrobial activities [4], although no parallel studies have been performed in healthy young children. AM are also important in controlling responses to inhaled antigens.…”

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confidence: 99%

Alveolar macrophage immaturity in infants and young children

Grigg

Riedler²,

Robertson³

et al. 1999

Eur Respir J

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Very little is known about alveolar macrophage (AM) immunological function in early childhood. Using nonbronchoscopic bronchoalveolar lavage (BAL), this study sought to compare the proportion, number, and function of AM between very young and older children.BAL fluid (BALF) leukocyte parameters were determined in 63 children, and data divided into 3 age groups: group 1 (<2 yrs), group 2 ($2±#5 yrs) and group 3 ($6± #17 years). In a further subgroup of children, AM function and immune receptor expression were assessed, and data categorized into two age groups: <2 yrs and $2 yrs of age.Compared to groups 2 and 3, the AM percentage in the BAL in group 1 was significantly increased (median: 98% versus 92% and 91%), as was the albuminadjusted AM concentration. AM from children <2 yrs expressed less human leukocyte antigen (HLA)-DR (versus $2 yrs of age), were less effective in reducing nitro blue tetrazolium, and released less interleukin (IL)-1 and tumour necrosis factor on lipopolysaccharide stimulation. There was no difference in release of IL-6, expression of intercellular adhesion molecule-1 (CD54), and AM stimulation of allogeneic T-cells, between children <2 yrs and $2 yrs of age.It was concluded that the capacity of alveolar macrophage to stimulate T-cells is not enhanced in early childhood, and that immaturity of alveolar macrophage function may contribute to an increased susceptibility to respiratory infections in this age group.

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“…When compared with the adult, the newborn macrophage functions of chemotaxis, phagocytosis, and bacterial killing are diminished (23)(24)(25). GSH is essential for optimal functioning of phagocytic cells, such as the alveolar macrophage.…”

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confidence: 99%

Fetal Alcohol Exposure Impairs Alveolar Macrophage Function via Decreased Glutathione Availability

et al. 2005

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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 ethanolexposed 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. Fetal alcohol exposure remains a significant problem in our society. Alcohol abuse and binge drinking by pregnant women has been estimated at an alarming 35% of pregnancies (1-3). Fetal alcohol syndrome or alcohol-related neurodevelopmental disorder has been estimated to occur in ‫0001/1ف‬ pregnancies (4). Because there is a strong relationship between cocaine abuse and concurrent alcohol ingestion (5-7), and both substances may increase the risk of premature delivery (7,8), a significant population of premature infants is exposed to alcohol in utero.In animal models of fetal alcohol exposure, alcohol increases systemic oxidative stress in the developing fetus (9 -14). A decrease in the antioxidant GSH has been demonstrated, particularly in the alcohol-exposed fetal liver (9,15,16). As an essential antioxidant in the body, GSH is normally present in high concentrations in the ELF of the lung (17). The fetal lung is at risk for increased oxidative stress during development, because maturation of antioxidant systems, including GSH, is gestationally dependent (18,19). A reduction in alveolar GSH, as seen in the premature infant, leaves the preterm lung susceptible to increased pulmonary oxidative injury (20,21) and chronic lung disease (18,22). The impact of the oxidative stress of fetal alcohol exposure superimposed on the low GSH environment of the developing lu...

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The Ontogeny of Pulmonary Defenses: Alveolar Macrophage Function in Neonatal and Juvenile Rhesus Monkeys

Cited by 63 publications

References 29 publications

Secretion of Transforming Growth Factor-α (TGFα) by Postnatal Rabbit Alveolar Macrophages

Secretion of Transforming Growth Factor-α (TGFα) by Postnatal Rabbit Alveolar Macrophages

Alveolar macrophage immaturity in infants and young children

Fetal Alcohol Exposure Impairs Alveolar Macrophage Function via Decreased Glutathione Availability

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