Intra-Amniotic Administration of E coli Lipopolysaccharides Causes Sustained Inflammation of the Fetal Skin in Sheep

Zhang, Li; Saito, Masatoshi; Jobe, Alan H.; Kallapur, Suhas G.; Newnham, John P.; Cox, Thomas; Kramer, Boris W.; Yang, Huixia; Kemp, Matthew W.

doi:10.1177/1933719112446079

Cited by 20 publications

(21 citation statements)

References 35 publications

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“…Total RNA was extracted from liquid nitrogen-homogenized fetal tissues (lung right lower lobe, axilla skin, chorioamnion, and spleen) using TRIzol (Life Technologies, Carlsbad, CA, USA) as previously described (40,41). Extracted RNA was treated with Turbo DNase (Life Technologies) in accordance with the manufacturer's instructions to remove any residual DNA.…”

Section: Methodsmentioning

confidence: 99%

Maternal Intravenous Treatment with either Azithromycin or Solithromycin Clears Ureaplasma parvum from the Amniotic Fluid in an Ovine Model of Intrauterine Infection

Miura

Payne

Keelan

et al. 2014

Antimicrob Agents Chemother

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Section: Methodsmentioning

confidence: 99%

Maternal Intravenous Treatment with either Azithromycin or Solithromycin Clears Ureaplasma parvum from the Amniotic Fluid in an Ovine Model of Intrauterine Infection

Miura

Payne

Keelan

et al. 2014

Antimicrob Agents Chemother

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“…A fetal inflammatory response in the lung was initiated within a few hours after intra-amniotic LPS delivery (21,23). In addition, 2 days after intra-amniotic LPS administration, proinflammatory cytokines and chemokines were detected in the ovine fetal skin (25,41).…”

mentioning

confidence: 97%

Chorioamnionitis-induced fetal gut injury is mediated by direct gut exposure of inflammatory mediators or by lung inflammation

Wolfs

Kramer

Thuijls

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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Wolfs TG, Kramer BW, Thuijls G, Kemp MW, Saito M, Willems MG, Senthamarai-Kannan P, Newnham JP, Jobe AH, Kallapur SG. Chorioamnionitis-induced fetal gut injury is mediated by direct gut exposure of inflammatory mediators or by lung inflammation. Am J Physiol Gastrointest Liver Physiol 306: G382-G393, 2014. First published January 23, 2014; doi:10.1152/ajpgi.00260.2013.-Intra-amniotic exposure to proinflammatory agonists causes chorioamnionitis and fetal gut inflammation. Fetal gut inflammation is associated with mucosal injury and impaired gut development. We tested whether this detrimental inflammatory response of the fetal gut results from a direct local (gut derived) or an indirect inflammatory response mediated by the chorioamnion/skin or lung, since these organs are also in direct contact with the amniotic fluid. The gastrointestinal tract was isolated from the respiratory tract and the amnion/ skin epithelia by fetal surgery in time-mated ewes. Lipopolysaccharide (LPS) or saline (controls) was selectively infused in the gastrointestinal tract, trachea, or amniotic compartment at 2 or 6 days before preterm delivery at 124 days gestation (term 150 days). Gastrointestinal and intratracheal LPS exposure caused distinct inflammatory responses in the fetal gut. Inflammatory responses could be distinguished by the influx of leukocytes (MPO ϩ , CD3 ϩ , and FoxP3 ϩ cells), tumor necrosis factor-␣, and interferon-␥ expression and differential upregulation of mRNA levels for Toll-like receptor 1, 2, 4, and 6. Fetal gut inflammation after direct intestinal LPS exposure resulted in severe loss of the tight junctional protein zonula occludens protein 1 (ZO-1) and increased mitosis of intestinal epithelial cells. Inflammation of the fetal gut after selective LPS instillation in the lungs caused only mild disruption of ZO-1, loss in epithelial cell integrity, and impaired epithelial differentiation. LPS exposure of the amnion/skin epithelia did not result in gut inflammation or morphological, structural, and functional changes. Our results indicate that the detrimental consequences of chorioamnionitis on fetal gut development are the combined result of local gut and lung-mediated inflammatory responses.endotoxin; fetal inflammatory response; necrotizing enterocolitis; sheep A FREQUENT ASSOCIATION WITH preterm delivery is chorioamnionitis, a bacterial infection of the amniotic fluid, fetal membranes, and placenta (13,28,30). Chorioamnionitis is associated with an increased risk for poor postnatal developmental outcomes (3,4,15,32). The inflammatory response to chorioamnionitis is postulated to be the proximal cause of injury to fetal organs, which increase the risk of periventricular leukomalacia (6) necrotizing enterocolitis (3, 4), and bronchopulmonary dysplasia (34, 37). Because the fetus swallows and aspirates the amniotic fluid, infection of the amniotic fluid exposes the premature lungs and intestine directly to bacteria and inflammatory products. In addition, the fetal skin and the amniotic epithelium are exposed to...

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“…The fetus inspires, swallows, and is bathed in amniotic fluid; therefore, the fetal lungs (68,69), gastrointestinal tract (70,71), and skin (72) are primary sites of inflammation-mediated injury. Exposure to inflammatory mediators may also occur via the placental-fetal circulation, resulting in immunomodulation within the fetal blood (73)(74)(75), lymphoid tissues (76)(77)(78), and distant organs such as the brain (79,80).…”

Section: Neonatal Sequelae Of Chorioamnionitismentioning

confidence: 99%

The Human Ureaplasma Species as Causative Agents of Chorioamnionitis

et al. 2017

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SUMMARY The human Ureaplasma species are the most frequently isolated microorganisms from the amniotic fluid and placentae of women who deliver preterm and are also associated with spontaneous abortions or miscarriages, neonatal respiratory diseases, and chorioamnionitis. Despite the fact that these microorganisms have been habitually found within placentae of pregnancies with chorioamnionitis, the role of Ureaplasma species as a causative agent has not been satisfactorily explained. There is also controversy surrounding their role in disease, particularly as not all women infected with Ureaplasma spp. develop chorioamnionitis. In this review, we provide evidence that Ureaplasma spp. are associated with diseases of pregnancy and discuss recent findings which demonstrate that Ureaplasma spp. are associated with chorioamnionitis, regardless of gestational age at the time of delivery. Here, we also discuss the proposed major virulence factors of Ureaplasma spp., with a focus on the multiple-banded antigen (MBA), which may facilitate modulation/alteration of the host immune response and potentially explain why only subpopulations of infected women experience adverse pregnancy outcomes. The information presented within this review confirms that Ureaplasma spp. are not simply “innocent bystanders” in disease and highlights that these microorganisms are an often underestimated pathogen of pregnancy.

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Intra-Amniotic Administration of E coli Lipopolysaccharides Causes Sustained Inflammation of the Fetal Skin in Sheep

Cited by 20 publications

References 35 publications

Maternal Intravenous Treatment with either Azithromycin or Solithromycin Clears Ureaplasma parvum from the Amniotic Fluid in an Ovine Model of Intrauterine Infection

Maternal Intravenous Treatment with either Azithromycin or Solithromycin Clears Ureaplasma parvum from the Amniotic Fluid in an Ovine Model of Intrauterine Infection

Chorioamnionitis-induced fetal gut injury is mediated by direct gut exposure of inflammatory mediators or by lung inflammation

The Human Ureaplasma Species as Causative Agents of Chorioamnionitis

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