Oral, nasal and pharyngeal exposure to lipopolysaccharide causes a fetal inflammatory response in sheep.

Oral, nasal and pharyngeal exposure to lipopolysaccharide causes a fetal inflammatory response in sheep.
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DOI:
10.1371/journal.pone.0119281
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发表时间:
2015
期刊:
影响因子:
3.7
通讯作者:
Kallapur SG
Kallapur SG
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Maneenil G;Kemp MW;Kannan PS;Kramer BW;Saito M;Newnham JP;Jobe AH;Kallapur SG

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绵羊胎儿炎症反应(FIR)可由羊膜内或选择性暴露于胎儿肺或肠道脂多糖(LPS)引起。口腔、鼻腔和咽腔(ONP)含有与羊水接触的淋巴组织和上皮。ONP上皮和淋巴组织启动FIR的能力尚不清楚。确定胎羊选择性ONP暴露于LPS后是否发生FIR。采用胎儿恢复手术,我们通过气管和食管结扎并在鼻部戴上闭塞手套,从胎儿肺、胃肠道和羊水中分离出ONP。LPS (5 mg)或生理盐水注入24 h Alzet泵固定于口腔内(n = 7-8 /组)。动物在LPS或生理盐水输注后1或6天分娩。暴露于LPS的ONP具有时间依赖性的全身性炎症效应,包括脐带血白细胞的改变,6天后后纵隔淋巴结重量的增加,以及胎儿血浆、肺和肝脏中促炎mRNA的反应。与对照组相比,ONP暴露于LPS后第1天和第6天表面活性剂蛋白A mRNA的表达增加。ONP单独暴露于LPS可在未直接暴露于LPS的远端胎儿组织中诱导轻度FIR伴时间依赖性炎症反应。
A 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. To determine if FIR occurs after selective ONP exposure to LPS in fetal sheep. Using 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. The 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. ONP exposure to LPS alone can induce a mild FIR with time-dependent inflammatory responses in remote fetal tissues not directly exposed to LPS.
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