2001
DOI: 10.1067/mob.2001.13321
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Chorioamnionitis and inflammation of the fetal lung

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Cited by 73 publications
(52 citation statements)
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“…Second, pMw also may be recruited to other sites of fetal inflammation, such as the fetal lungs or membranes, especially in cases of infection of the fetus or amniotic fluid. Supporting this hypothesis, increased numbers of CD68 + macrophages have been reported in fetal lungs during CA (55). The most striking finding of the immunohistochemical analysis in CA patients was the increased expression of CD163 in stage III placentas as compared with stage II placentas and in those with documented infection.…”
Section: Discussionsupporting
confidence: 56%
“…Second, pMw also may be recruited to other sites of fetal inflammation, such as the fetal lungs or membranes, especially in cases of infection of the fetus or amniotic fluid. Supporting this hypothesis, increased numbers of CD68 + macrophages have been reported in fetal lungs during CA (55). The most striking finding of the immunohistochemical analysis in CA patients was the increased expression of CD163 in stage III placentas as compared with stage II placentas and in those with documented infection.…”
Section: Discussionsupporting
confidence: 56%
“…7 This inflammatory response may be initiated antenatally by chorioamnionitis and/or sustained by postnatal interventions such as resuscitation, oxygen toxicity and mechanical ventilation with baro-or volutrauma. [8][9][10] This hypothesis was derived from the analyses of tracheal aspirates from ventilated preterm babies and lung tissue from preterm infants who died. [10][11][12] Few large studies have correlated chorioamnionitis with lung outcomes.…”
Section: Antenatal Inflammationmentioning
confidence: 99%
“…31 A pronounced IL-8 mRNA-expression could also be detected in the bronchoalveolar epithelium and in a scattered pattern in the interstitial tissue of post-mortem lung tissue of infants with RDS. 32 The increased levels and enhanced mRNA expression of proinflammatory cytokines present in the airways and pulmonary tissue of preterm infants may reflect an inability to regulate inflammation through an adequate expression of the antiinflammatory cytokines IL-10, IL-4, IL-12 and IL-13 or IL-1 receptor antagonist. 26,33 -35 Cellular IL-10 mRNA was undetectable in most airway samples of preterm infants with RDS, but it was expressed in all cell samples of term infants with meconium aspiration syndrome.…”
Section: Inflammatory Cells Endothelial Interactions and Chemotaxismentioning
confidence: 99%
“…48 By now, a pronounced inflammatory response reflected by a marked infiltration of inflammatory cells, increased expression of IL-8 mRNA, and increased apoptosis, has been demonstrated in lung tissue of human fetuses exposed to chorioamnionitis. 32,49 Epidemiological data suggest a strong association between chorioamnionitis and the development of BPD, and increased concentrations of proinflammatory cytokines in human amniotic fluid and fetal cord blood -indicating a systemic inflammatory response during chorioamnionitis -were shown to be an independent risk factor for the development of BPD. 50,51 Furthermore, chorioamnionitis, mechanical ventilation, and postnatal sepsis have clearly been identified as modulators of BPD.…”
Section: Inflammatory Cells Endothelial Interactions and Chemotaxismentioning
confidence: 99%