ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Airway inflammatory cell responses to intra-amniotic lipopolysaccharide in a sheep model of chorioamnionitis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Investigating pulmonary inflammation and injury after progressive systemic inflammation in preterm fetal sheep.Frontiers in physiology · 2025Article
- Bacteria in the amniotic fluid without inflammation: early colonization vs. contamination.Journal of perinatal medicine · 2021Article
- Sex-differences in LPS-induced neonatal lung injury.Scientific reports · 2019Article
- Inhibition of IκBβ/NFκB signaling prevents LPS-induced IL1β expression without increasing apoptosis in the developing mouse lung.Pediatric research · 2017Article
- Brief mechanical ventilation causes differential epithelial repair along the airways of fetal, preterm lambs.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Distending Pressure Did Not Activate Acute Phase or Inflammatory Responses in the Airways and Lungs of Fetal, Preterm Lambs.PloS one · 2016Article
- Lipopolysaccharide and soluble CD14 in cord blood plasma are associated with prematurity and chorioamnionitis.Pediatric research · 2014Article
- Preterm birth, intrauterine infection, and fetal inflammation.Frontiers in immunology · 2014Review
- Effects of chorioamnionitis on the fetal lung.Clinics in perinatology · 2012Review
- Interleukin-19 in fetal systemic inflammation.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2012Article
- Intra-amniotic LPS and antenatal betamethasone: inflammation and maturation in preterm lamb lungs.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Positive end-expiratory pressure and surfactant decrease lung injury during initiation of ventilation in fetal sheep.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Chronic fetal exposure to Ureaplasma parvum suppresses innate immune responses in sheep.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Targeting inflammation to prevent bronchopulmonary dysplasia: can new insights be translated into therapies?Pediatrics · 2011Review
- Inhibitors of inflammation and endogenous surfactant pool size as modulators of lung injury with initiation of ventilation in preterm sheep.Respiratory research · 2010Article
- Chorioamnionitis: a multiorgan disease of the fetus?Journal of perinatology : official journal of the California Perinatal Association · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Chorioamnionitis, a risk factor for bronchopulmonary dysplasia in preterm infants, causes an influx of inflammatory cells into the fetal lung. Using a fetal sheep model, we evaluated the time course of activation, functional maturity, and apoptosis of the leukocytes recruited to the fetal air spaces by lipopolysaccharide (LPS). Time-mated sheep were given intra-amniotic injections with 10 mg of Escherichia coli LPS or saline 2 or 7 days before preterm delivery at 124 days of gestation (term is 150 days). Both neutrophils and monocytes in bronchoalveolar lavage fluid (BALF) had activated NF-kappaB after 2- and 7-day LPS exposures. These neutrophils and monocytes expressed the activation factor CD11b and the maturation factor PU.1 at 2 days, and increased PU.1 expression was detected in macrophages at 7 days. Leukocyte oxidative burst activity was greatest at 7 days. BALF lipid peroxidation increased fivefold at 2 days, while protein carbonyls increased eightfold at 7 days. Nitrative stress was not detected in the BALF, but leukocytes in the lung expressed nitric oxide synthase (NOS)II (inducible NOS). BALF leukocytes expressed the antioxidant peroxiredoxin V. Lung glutathione peroxidase was also increased with LPS exposure. There was minimal apoptosis of airway and lung leukocytes assessed by caspase-3 activation. Intra-amniotic LPS recruits leukocytes to the fetal air space that have a persistent activation. These results have implications for the pathogenesis of lung inflammatory disorders in the preterm.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.