Abstract
Background and aims: Exposure of the fetus to antenatal inflammation can occur from chorioamnionitis which may progress to a systemic fetal inflammatory response syndrome (FIRS). It is not known whether the fetal myocardium participates in this FIRS. We hypothesized that the myocardium would have indicators of inflammation and injury.Methods: Fetal sheep were exposed to intra-amniotic (IA) endotoxin or saline 2d or 7d before preterm delivery at 124 ± 1 days gestational age of gestation (term 150 days). Protein and mRNA levels in hearts were determined by real-time PCR, Western blotting and immunohistochemistry.Results: After IA exposure 2d before delivery, mRNA decreased compared to controls (100%) for hypoxia-inducible factor (HIF)-1α (18%), inducible NO-synthase (iNOS) (5%), toll-like receptor 2 (TLR2) (12%) and TLR4 (16%). Interleukin (IL)-6 mRNA increased to 146% after 2d and 390% after 7d. Protein levels of phosphorylated signal transducer and activator of transcription (STAT)-3 were decreased to 37% after 7d. HIF-1α protein level in cardiomyocytes decreased to 17 % after 2d. Fetal plasma level of cardiac troponin I decreased at both time points (21%, 47%).Conclusions: Acute (2d) endotoxin-induced chorioamnionitis suppressed mediators of cellular inflammatory response whereas a 7d exposure to endotoxin caused mild cardiac inflammation. There was no indication of severe cardiac injury.
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