Intra-amniotic Infection Upregulates Neutrophil Gelatinase-Associated Lipocalin (NGAL) Expression at the Maternal-Fetal Interface at Term

Tadesse, Serkalem; Luo, Guoyang; Park, Joong Shin; Kim, Byoung Jae; Snegovskikh, Victoria; Zheng, Ting; Hodgson, Eric J.; Arcuri, Felice; Toti, Paolo; Parikh, Chirag R.; Guller, Seth; Norwitz, Errol R.

doi:10.1177/1933719110396722

Cited by 34 publications

(33 citation statements)

References 33 publications

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“…dysfunctional endothelium [9,13], or alternatively, due to a local production in the placenta. Thus, it would be worth examining the production of NGAL in placentas from preeclamptic pregnancies, as NGAL has been detected in trophoblast cells with up-regulated expression in intraamniotic infection [19]. Metalloproteinase 9 (MMP9) is up-regulated in human placenta from women with preeclampsia [20].…”

Section: Discussionmentioning

confidence: 99%

Urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion increases in normal pregnancy but not in preeclampsia

Ødum

Andersen²,

Hviid

2014

Clinical Chemistry and Laboratory Medicine (CCLM)

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Section: Discussionmentioning

confidence: 99%

Urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion increases in normal pregnancy but not in preeclampsia

Ødum

Andersen²,

Hviid

2014

Clinical Chemistry and Laboratory Medicine (CCLM)

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“…NGAL is a host protein that participates in nutritional immunity as well as transport of various substances including iron, prostaglandins and MMPs [48]. NGAL was occasionally observed in DSCs without significant increase during infection (less frequent than trophoblasts) [48]. No significant change was detected in DSC NGAL expression after exposure to LPS, TNF-α or IL-1β [48].…”

Section: Methodsmentioning

confidence: 99%

Current concepts in maternal-fetal immunology: Recognition and response to microbial pathogens by decidual stromal cells

Anders

Gaddy

Doster

et al. 2017

Am J Reprod Immunol

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Chorioamnionitis is an acute inflammation of the gestational (extraplacental) membranes, most commonly caused by ascending microbial infection. It is associated with adverse neonatal outcomes including preterm birth, neonatal sepsis and cerebral palsy. The decidua is the outermost layer of the gestational membranes and is likely an important initial site of contact with microbes during ascending infection. However, little is known about how decidual stromal cells (DSCs) respond to microbial threat. Defining the contributions of individual cell types to the complex medley of inflammatory signals during chorioamnionitis could lead to improved interventions aimed at halting this disease. We review available published data supporting the role for DSCs in responding to microbial infection, with a special focus on their expression of pattern recognition receptors and evidence of their responsiveness to pathogen sensing. While DSCs likely play an important role in sensing and responding to infection during the pathogenesis of chorioamnionitis, important knowledge gaps and areas for future research are highlighted.

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“…Elegant, albeit indirect, studies using transgenic mice lacking cytokine receptors for IL-4 or IL-13, pregnant with wild-type (heterozygous) offspring, showed that maternal injection with receptor ligands had no effect on cytokine receptor signaling in fetal tissues, strongly suggesting that IL-4 and IL-13 do not cross the placenta (28). Instead, circulating maternal signaling molecules (e.g., cytokines, "alarmins," hyaluronan) may stimulate placental production of proinflammatory cytokines that contribute to altered development in the fetus and offspring (29). Exposures in early pregnancy could also have effects on fetal imprinting, altering immune responses by epigenetic mechanisms, a pathway of considerable interest, given the direct evidence in experimental asthma (30,31) and the suggestive associations reported in human asthma (32).…”

Section: Discussionmentioning

confidence: 99%

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

Auten¹,

Gilmour

Krantz

et al. 2012

Am J Respir Cell Mol Biol

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Air pollutant exposure is linked with childhood asthma incidence and exacerbations, and maternal exposure to airborne pollutants during pregnancy increases airway hyperreactivity (AHR) in offspring. To determine if exposure to diesel exhaust (DE) during pregnancy worsened postnatal ozone-induced AHR, timed pregnant C57BL/6 mice were exposed to DE (0.5 or 2.0 mg/m 3 ) 4 hours daily from Gestation Day 9-17, or received twice-weekly oropharyngeal aspirations of the collected DE particles (DEPs). Placentas and fetal lungs were harvested on Gestation Day 18 for cytokine analysis. In other litters, pups born to dams exposed to air or DE, or to dams treated with aspirated diesel particles, were exposed to filtered air or 1 ppm ozone beginning the day after birth, for 3 hours per day, 3 days per week for 4 weeks. Additional pups were monitored after a 4-week recovery period. Diesel inhalation or aspiration during pregnancy increased levels of placental and fetal lung cytokines. There were no significant effects on airway leukocytes, but prenatal diesel augmented ozone-induced elevations of bronchoalveolar lavage cytokines at 4 weeks. Mice born to the high-concentration dieselexposed dams had worse ozone-induced AHR, which persisted in the 4-week recovery animals. Prenatal diesel exposure combined with postnatal ozone exposure also worsened secondary alveolar crest development. We conclude that maternal inhalation of DE in pregnancy provokes a fetal inflammatory response that, combined with postnatal ozone exposure, impairs alveolar development, and causes a more severe and long-lasting AHR to ozone exposure.Keywords: diesel; fetal inflammation; ozone; airway hyperreactivity Increasing asthma prevalence among children in industrialized nations has stimulated a number of investigations focused on early life exposures to air pollutants (1). Maternal exposures to a variety of inhaled atmospheric pollutants, including side and mainstream tobacco smoke, diesel exhaust (DE), and ozone, have been linked in epidemiologic studies to asthma and other respiratory diseases in children (2-4). Animal models aimed at deciphering the mechanisms by which maternal exposures during pregnancy are linked to childhood asthma have largely focused on pathways relevant to allergic asthma (5).In addition to allergic sensitization, in utero exposure to air pollutants may also affect nonspecific pulmonary responses, such as airway hyperreactivity (AHR) (6). It has already been shown that fetal pulmonary inflammatory challenges are linked with impaired postnatal alveolar development (7-9), which affects airway stability and AHR (10). Previous studies have shown that maternal exposure to DE during pregnancy modified mouse placental cytokines relevant to airway inflammation (11), and lowered the threshold for AHR in ovalbuminsensitized offspring (12).We have previously shown that a standardized urban particulate delivered by oropharyngeal aspiration during pregnancy induced placental inflammatory cytokine expression and worsened neonatal ozone-induced...

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Intra-amniotic Infection Upregulates Neutrophil Gelatinase-Associated Lipocalin (NGAL) Expression at the Maternal-Fetal Interface at Term

Cited by 34 publications

References 33 publications

Urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion increases in normal pregnancy but not in preeclampsia

Urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion increases in normal pregnancy but not in preeclampsia

Current concepts in maternal-fetal immunology: Recognition and response to microbial pathogens by decidual stromal cells

Maternal Diesel Inhalation Increases Airway Hyperreactivity in Ozone-Exposed Offspring

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