Abstract
BackgroundA fetal inflammatory response (FIR) in sheep can be induced by intraamniotic or selective exposure of the fetal lung or gut to lipopolysaccharide (LPS). The oral, nasal, and pharyngeal cavities (ONP) contain lymphoid tissue and epithelium that are in contact with the amniotic fluid. The ability of the ONP epithelium and lymphoid tissue to initiate a FIR is unknown.ObjectiveTo determine if FIR occurs after selective ONP exposure to LPS in fetal sheep.MethodsUsing fetal recovery surgery, we isolated ONP from the fetal lung, GI tract, and amniotic fluid by tracheal and esophageal ligation and with an occlusive glove fitted over the snout. LPS (5 mg) or saline was infused with 24 h Alzet pumps secured in the oral cavity (n = 7–8/group). Animals were delivered 1 or 6 days after initiation of the LPS or saline infusions.ResultsThe ONP exposure to LPS had time-dependent systemic inflammatory effects with changes in WBC in cord blood, an increase in posterior mediastinal lymph node weight at 6 days, and pro-inflammatory mRNA responses in the fetal plasma, lung, and liver. Compared to controls, the expression of surfactant protein A mRNA increased 1 and 6 days after ONP exposure to LPS.ConclusionONP exposure to LPS alone can induce a mild FIR with time-dependent inflammatory responses in remote fetal tissues not directly exposed to LPS.
Highlights
Chorioamnionitis is commonly associated with preterm delivery [1]
We isolated ONP from the fetal lung, GI tract, and amniotic fluid by tracheal and esophageal ligation and with an occlusive glove fitted over the snout
ONP exposure to LPS alone can induce a mild fetal inflammatory response (FIR) with time-dependent inflammatory responses in remote fetal tissues not directly exposed to LPS
Summary
Chorioamnionitis is commonly associated with preterm delivery [1]. Chorioamnionitis can increase the expression of cytokines and chemokines within the gestational tissues and stimulate the production of prostaglandins, causing uterine contraction and preterm delivery [2]. The fetus can respond to infection and inflammation in the amniotic fluid with a fetal inflammatory response (FIR) that can be detected by increased IL-6 levels in cord plasma or by inflammation in the umbilical cord, termed funisitis [3,4]. Selective exposures to the gut or lung were achieved by ligating the trachea or esophagus with organ targeted exposure to the agonists, while a selective skin/chorioamnion exposure was achieved by occluding the mouth and nose of the fetus [20] For these previously reported experiments, the oral, nasal, and pharyngeal (ONP) epithelial and lymphoid tissues were excluded from agonist exposure. The ability of the ONP epithelium and lymphoid tissue to initiate a FIR is unknown.
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