Chronic Hypoxemia Absent Bacterial Infection Is One Cause of the Fetal Inflammatory Response Syndrome (FIRS)

Dong, Yafeng; Hou, Wei; Wei, Jiaxue; Weiner, Carl P.

doi:10.1177/1933719109333662

Cited by 21 publications

(21 citation statements)

References 34 publications

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“…Thus, it is reasonable to speculate that inflammation plays a role in the pathogenesis of perinatal brain injury. We demonstrated that chronic hypoxia increases IL-6 and TNF-α in fetal blood of guinea pig, fulfilling the diagnostic criteria in humans for fetal inflammatory response syndrome 13. This inflammatory response is highly associated with both spontaneous preterm birth and subsequent neurodevelopmental compromise 14,15.…”

Section: Introductionmentioning

confidence: 62%

“…We have previously shown that this model of chronic fetal hypoxia generates inflammatory response in fetal multiple organs including the brain13, 44. This response is unique to the fetus as the brain of the dam is unaffected.…”

Section: Commentmentioning

confidence: 86%

“…This inflammatory response is highly associated with both spontaneous preterm birth and subsequent neurodevelopmental compromise 14,15. Chronic hypoxia also increased the expression of these cytokines in multiple fetal organs including the brain 13. And while there is extensive evidence linking acute perinatal ischemia 16 to proinflammatory cytokine and reactive oxygen species (ROS) generation 17, no such association has been identified for the more common clinical condition associated with neurodevelopmental compromise, chronic fetal hypoxia due to placental dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Chronic fetal hypoxia produces selective brain injury associated with altered nitric oxide synthases

Dong

Sun

et al. 2011

American Journal of Obstetrics and Gynecology

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OBJECTIVE The impact of chronic hypoxia on the nitric oxide synthase isoenzymes (NOSs) in specific brain structures is unknown. STUDY DESIGN Time-mated pregnant guinea pigs were exposed to 10.5% O2 for 14d (HPX) or room air (NMX); L-NIL (an iNOS inhibitor, 1mg/kg/day) was administered to HPX animals for 14d (L-NIL+HPX). Fetal brains were harvested at term. Multi-labeled immunofluorescence was used to generate a brain injury map. Laser capture microdissection and quantitative PCR were applied and cell injury markers, apoptosis activation, neuron loss, total NO, and the levels of individual NOSs quantified. RESULTS Chronic hypoxia causes selective fetal brain injury rather than globally. Injury is associated with differentially affected NO synthases in both neurons and glial cells, with iNOS up regulated at all injury sites. L-NIL attenuated the injury despite continued hypoxia. CONCLUSIONS These studies demonstrate chronic hypoxia selectively injures the fetal brain in part by the differential regulation of NOSs in an anatomic and cell specific manner.

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Section: Introductionmentioning

confidence: 62%

Section: Commentmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

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Chronic fetal hypoxia produces selective brain injury associated with altered nitric oxide synthases

Dong

Sun

et al. 2011

American Journal of Obstetrics and Gynecology

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“…A consequence of severe or prolonged fetal hypoxia is brain cellular damage, thought to be due to oxygen starvation and a secondary inflammatory response 2, 3 . Less is known about the cellular response to hypoxia of short duration.…”

Section: Introductionmentioning

confidence: 99%

Post-hypoxia Invasion of the fetal brain by multidrug resistant Staphylococcus

Zarate

Rodriguez

Chang

et al. 2017

Sci Rep

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Herein we describe an association between activation of inflammatory pathways following transient hypoxia and the appearance of the multidrug resistant bacteria Staphylococcus simulans in the fetal brain. Reduction of maternal arterial oxygen tension by 50% over 30 min resulted in a subseiuent significant over-expression of genes associated with immune responses 24 h later in the fetal brain. The activated genes were consistent with stimulation by bacterial lipopolysaccharide; an influx of macrophages and appearance of live bacteria were found in these fetal brains. S. simulans was the predominant bacterial species in fetal brain after hypoxia, but was found in placenta of all animals. Strains of S. simulans from the placenta and fetal brain were equally highly resistant to multiple antibiotics including methicillin and had identical genome sequences. These results suggest that bacteria from the placenta invade the fetal brain after maternal hypoxia.

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“…Moreover, ischemia and/or hypoxemia can also elicit changes that resemble systemic inflammation. Guinea pigs subjected to chronic hypoxemia have dramatically elevated levels of IL-6 and tumor necrosis factor-α concentrations in fetal blood [145]. This observation led the authors to propose that FIRS may be an adaptive response of the fetus to chronic hypoxemia.…”

Section: Introductionmentioning

confidence: 99%

Blood pH and gases in fetuses in preterm labor with and without systemic inflammatory response syndrome

Romero¹,

Soto²,

Berry³

et al. 2011

The Journal of Maternal-Fetal & Neonatal Medicine

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OBJECTIVE Fetal hypoxemia has been proposed to be one of the mechanisms of preterm labor (PTL) and delivery. This may have clinical implications since it may alter: 1) the method/frequency of fetal surveillance; and 2) the indications and duration of tocolysis to an already compromised fetus. The aim of this study was to examine whether there is a difference in the fetal blood gas analysis [pH, PaO2 and base excess (BE)] and in the prevalence of fetal acidemia and hypoxia between: 1) patients in PTL who delivered within 72 hours vs. those who delivered more than 72 hours after cordocentesis; and 2) patients with Fetal Inflammatory Response Syndrome (FIRS) vs. those without this condition. STUDY DESIGN Patients admitted with PTL underwent amniocentesis and cordocentesis. Ninety women with singleton pregnancies and PTL were classified according to 1) those who delivered within 72 hours (n = 30) and after 72 hours of the cordocentesis (n = 60); and 2) with and without FIRS. FIRS was defined as a fetal plasma concentration of IL-6 >11 pg/mL. Fetal blood gases were determined. Acidemia and hypoxemia were defined as fetal pH and PaO2 below the 5th percentile for gestational age, respectively. For comparisons between the two study groups, ΔpH and ΔPaO2 were calculated by adjusting for gestational age (Δ = observed value-mean for gestational age). Non-parametric statistics were employed. RESULTS No differences in the median Δ pH (−0.026 vs. −0.016), ΔPaO2 (0.25 mmHg vs. 5.9 mmHg) or BE (−2.4 mEq/L vs. −2.6 mEq/L) were found between patients with PTL who delivered within 72 hours and those who delivered 72 hours after the cordocentesis (p>0.05 for all comparisons). Fetal plasma IL-6 concentration was determined in 63% (57/90) of fetuses and the prevalence of FIRS was 28% (16/57). There was no difference in fetal pH, PaO2 and BE between fetuses with and without FIRS (p>0.05 for all comparisons). Moreover, there was no difference in the rate of fetal acidemia between fetuses with and without FIRS (6.3% vs. 9.8%; p>0.05) and fetal hypoxia between fetuses with or without FIRS (12.5% vs. 19.5%; p>0.05). CONCLUSIONS Our data do not support a role for acute fetal hypoxemia and metabolic acidemia in the etiology of preterm labor and delivery.

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Chronic Hypoxemia Absent Bacterial Infection Is One Cause of the Fetal Inflammatory Response Syndrome (FIRS)

Cited by 21 publications

References 34 publications

Chronic fetal hypoxia produces selective brain injury associated with altered nitric oxide synthases

Chronic fetal hypoxia produces selective brain injury associated with altered nitric oxide synthases

Post-hypoxia Invasion of the fetal brain by multidrug resistant Staphylococcus

Blood pH and gases in fetuses in preterm labor with and without systemic inflammatory response syndrome

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