OBJECTIVES Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations may be contributing to heightened immune signals that have the potential to disrupt neuronal homeostasis and exacerbate behavioural deficits. The current study aimed to determine whether the well-characterized animal model of neuropsychopathology, the maternal immune activation (MIA) model, produced GI inflammation and integrity disruptions in association with anxiety-like behaviour. METHODS Pregnant Wistar rats were exposed to the viral mimetic polyriboinosinic:polyribocytidilic acid (polyI:C) on gestational days (GD) 10 and 19. Evidence of ANS activation, GI inflammation, and GI barrier integrity was assessed in both neonatal (postnatal day, P7) and adult (P84) offspring. Anxiety-like behaviour was assessed at P100. RESULTS Neonatal MIA offspring exhibited an altered intestinal inflammatory profile and evidence of an increase in lymphoid aggregates. MIA neonates also displayed disruptions to GI barrier tight junction protein mRNA. In addition, adult MIA offspring exhibited an increase in anxiety-like behaviours. CONCLUSION These results indicate that the MIA rat model, which is well documented to produce behavioural, neurochemical, and neuroanatomical abnormalities, also produces GI inflammation and integrity disruptions. We suggest that this model may be a useful tool to elucidate biological pathways associated with neuropsychiatric disorders.

中文翻译：

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啮齿动物焦虑模型：围产期免疫挑战对胃肠道炎症和完整性的影响。

目的胃肠道（GI）炎症和胃肠道完整性缺陷是神经精神疾病的常见合并症。正在进行的研究表明，这些畸变可能会增强免疫信号，从而可能破坏神经元稳态并加剧行为缺陷。当前的研究旨在确定神经心理病理学的特征鲜明的动物模型，母体免疫激活（MIA）模型是否会产生与焦虑样行为相关的胃肠道炎症和完整性破坏。方法妊娠Wistar大鼠在妊娠第10天和第19天暴露于病毒模拟的多核糖肌酸：多核糖核酸（polyI：C），并评估了新生儿（产后，出生后）的ANS活化，胃肠道炎症和胃肠道屏障完整性的证据。 P7）和成年（P84）后代。在P100评估了焦虑样行为。结果新生儿MIA后代表现出肠道炎症特征的改变和淋巴样聚集物增加的证据。MIA新生儿还显示了对胃肠道屏障紧密连接蛋白mRNA的破坏。此外，成年MIA后代表现出焦虑样行为的增加。结论这些结果表明，MIA大鼠模型已被证明可产生行为，神经化学和神经解剖学异常，也可产生胃肠道炎症和完整性破坏。我们建议该模型可能是阐明与神经精神疾病相关的生物学途径的有用工具。结果新生儿MIA后代表现出肠道炎症特征的改变和淋巴样聚集物增加的证据。MIA新生儿还显示了对胃肠道屏障紧密连接蛋白mRNA的破坏。此外，成年MIA后代表现出焦虑样行为的增加。结论这些结果表明，MIA大鼠模型已被证明可产生行为，神经化学和神经解剖学异常，也可产生胃肠道炎症和完整性破坏。我们建议该模型可能是阐明与神经精神疾病相关的生物学途径的有用工具。结果新生儿MIA后代表现出肠道炎症特征的改变和淋巴样聚集物增加的证据。MIA新生儿还显示了对胃肠道屏障紧密连接蛋白mRNA的破坏。此外，成年MIA后代表现出焦虑样行为的增加。结论这些结果表明，MIA大鼠模型已被证明可产生行为，神经化学和神经解剖学异常，也可产生胃肠道炎症和完整性破坏。我们建议该模型可能是阐明与神经精神疾病相关的生物学途径的有用工具。结论这些结果表明，MIA大鼠模型已被证明可产生行为，神经化学和神经解剖学异常，也可产生胃肠道炎症和完整性破坏。我们建议该模型可能是阐明与神经精神疾病相关的生物学途径的有用工具。结论这些结果表明，MIA大鼠模型已被证明可产生行为，神经化学和神经解剖学异常，也可产生胃肠道炎症和完整性破坏。我们建议该模型可能是阐明与神经精神疾病相关的生物学途径的有用工具。