Regulation of macrophage functions in the murine placenta and decidua: Implications for tolerance of the fetal allograft

Lu, Christopher Y.; Redline, Raymond W.; McKay, Dianne B.; Dustin, Lynn B.; Shea, Colleen M.

doi:10.1016/s0955-470x(89)80013-8

Cited by 4 publications

(4 citation statements)

References 59 publications

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“…Others have shown that production of TNFot after stimulation by LPS in vitro is not inhibited by D H A (26). Our data may help explain the increased susceptibility of the fetus, neonate, and placenta to intracellular pathogens such as Listeria monocytogenes (27). The concentrations of DHA which inhibit NO production are present in neonatal and fetal serum (5,7) and those areas of the placenta perfused by the fetal circulation.…”

Section: Resultsmentioning

confidence: 54%

Transcription of the murine iNOS gene is inhibited by docosahexaenoic acid, a major constituent of fetal and neonatal sera as well as fish oils.

Khair‐El‐Din

Sicher

Vázquez

et al. 1996

The Journal of Experimental Medicine

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SummaryMacrophage activation is deficient in the fetus and neonate when the serum concentrations of docosahexaenoic acid (DHA) are 150 p.M, or 10-50-fold higher than in the adult. We now show that DHA inhibits production of nitric oxide (NO) by macrophages stimulated in vitro by IFN~/plus LPS, or by IFNy plus TNF~x. The half-maximal inhibitory activity of DHA was ,'~25 p~M. There were strict biochemical requirements of the fatty acid for inhibition. Polyenoic fatty acids with 22 carbons were more inhibitory than those with 20 carbons. Among 22-carbon fatty acids, those with a greater number of double bonds and a double bond in the n-3 position were more inhibitory. DHA was the most inhibitory of the polyenoic acids we tested.Inducible nitric oxide synthase (iNOS) is the enzyme responsible for the production of NO by macrophages. NO production is initiated after new iNOS enzyme is synthesized following transcription of the iNOS gene. In macrophages stimulated by IFN~/plus LPS, DHA inhibited accumulation ofiNOS mRNA, as measured by Northern blotting, and iNOS transcription, as measured by nuclear run-on assays. We transfected RAW 264.7 macrophages with a construct containing the iNOS promoter fused to the chloramphenicol acetyl transferase gene. DHA inhibited activation of this promoter by IFN~/plus LPS. By inhibiting iNOS transcription in the fetus and neonate, DHA may contribute to their increased susceptibility to infection.

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Section: Resultsmentioning

confidence: 54%

Transcription of the murine iNOS gene is inhibited by docosahexaenoic acid, a major constituent of fetal and neonatal sera as well as fish oils.

Khair‐El‐Din

Sicher

Vázquez

et al. 1996

The Journal of Experimental Medicine

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“…The placenta and fetus present a substantial challenge to the maternal immune system (Lu et al 1991). Vigorous local immune responses can potentially activate maternal anti-fetal allograft immunity but a less than adequate local immune response would allow pathogens to enter the placenta and gain access to an immature fetal immune system that is ill-prepared to respond to them.…”

Section: Acute Chorioamnionitismentioning

confidence: 99%

Placental Inflammation

Redline¹

2007

Fetal and Neonatal Pathology

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“…However, the listeriolysin virulence studies mentioned above employed adult rather than perinatal mice. Previous studies from this laboratory demonstrated that macrophage functions are profoundly inhibited in the murine neonate and decidua basalis, where the fetal placenta is anchored in the maternal uterus (21,23,24,32). Macrophages are an important effector cell in the host defense against Listeria infection (17), and these studies raise the possibility that in the setting of such inhibited macrophage functions, lysin-negative Listeria strains are pathogenic.…”

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confidence: 96%

Listeriolysin as a virulence factor in Listeria monocytogenes infection of neonatal mice and murine decidual tissue

McKay

1991

Infect Immun

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Listeriolysin is a 60-kDa protein which allows the growth of Listeria monocytogenes in macrophages and other cells and has been shown to be a virulence factor in Listeria infections of adult mice. However, the neonate and fetoplacental unit are major populations susceptible to listeriosis. Recent data indicate that macrophage and T-cell functions are markedly inhibited in these young mice, and the virulence of listeriolysin-negative (HLY-) and listeriolysin-positive (HLY+) Listeria cells in the setting of such inhibited macrophage and T-cell functions has not previously been examined. We now compare CNL 85/162, a transposon-induced, HLY- Listeria strain, and CNL 85/163, a spontaneous HLY+ revertant. We found that all 18 neonates injected with CNL 85/163 (HLY+) died within 12 days after an injection of 10(4) Listeria cells per mouse. In contrast, all 16 neonates injected with 1,000 times more CNL 85/162 (HLY-) cells survived more than 14 days. Three days after injection, growth of CNL 85/163 (HLY+) in the internal organs was more than 5 log greater than that of CNL 85/162 (HLY-). We also found that CNL 85/162 (HLY-) did not proliferate well in decidual tissue, which is a major component of the placental region. Our studies indicate that HLY- bacteria are not virulent in the neonate and the fetoplacental unit despite the inhibited immune functions at these sites.

show abstract

Regulation of macrophage functions in the murine placenta and decidua: Implications for tolerance of the fetal allograft

Cited by 4 publications

References 59 publications

Transcription of the murine iNOS gene is inhibited by docosahexaenoic acid, a major constituent of fetal and neonatal sera as well as fish oils.

Transcription of the murine iNOS gene is inhibited by docosahexaenoic acid, a major constituent of fetal and neonatal sera as well as fish oils.

Placental Inflammation

Listeriolysin as a virulence factor in Listeria monocytogenes infection of neonatal mice and murine decidual tissue

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