Journal
BIOLOGY OF THE NEONATE
Volume 88, Issue 3, Pages 202-207Publisher
KARGER
DOI: 10.1159/000087583
Keywords
innate immunity; respiratory distress syndrome; bronchopulmonary dysplasia; chorioamnionitis
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Funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD012714] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL065397] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL-65397] Funding Source: Medline
- NICHD NIH HHS [HD-12714] Funding Source: Medline
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Clinical and experimental information indicate that fetal exposure to inflammation can induce lung maturation. This inflammation may be chronic and indolent. We present clinical and experimental information that challenge assumptions about chorioamnionitis associated infection/inflammatory exposures to the fetus. We question the assumption that the fetal compartment is sterile, and that delivery is inevitable if chronic infection/inflammation is present. We demonstrate that the preterm fetus can develop a brisk and adequate inflammatory response, and the fetus also can quickly modulate and downregulate inflammation to prevent injury. The fetus at risk of early preterm delivery may be exposed to both chorioamnionitis and glucocorticoids. Both exposures can either increase or decrease fetal inflammatory responses depending on the timing of the exposures. The immunomodulatory ability of the fetus to fetal exposures remains an unexplored research field. Copyright (C) 2005 S. Karger AG, Basel.
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