Guidoni Pauline B, Pasternak J Alex, Hamonic Glenn, MacPhee Daniel J, Harding John C S
Department of Large Animal Clinical Sciences, University of Saskatchewan, Saskatoon, Canada.
Department of Animal Science, Purdue University, West Lafayette, USA.
Theriogenology. 2022 May;184:162-170. doi: 10.1016/j.theriogenology.2022.03.011. Epub 2022 Mar 14.
Understanding why intrauterine growth restricted (IUGR) fetuses are more resilient to transplacental porcine reproductive and respiratory syndrome virus-2 (PRRSV-2) infection compared to normal fetuses may lead to alternative approaches to control PRRS. Our objective was to compare gene expression of a subset of tight junction proteins in the endometrium (END) and placenta (PLC) of i) IUGR vs N-IUGR fetuses, and ii) across disease progression phenotypes following PRRSV-2 infection. In experiment 1, snap frozen END and PLC from fetuses of non-infected control dams (CTRL) and from high viral load viable (HVL-VIA) fetuses, with both groups further classified as either IUGR or non(N)-IUGR based on brain: liver weight ratio were strategically selected from a large challenge trial. In experiment 2, similar tissues were randomly selected from CTRL and from uninfected thymus (UNIF), (HVL-VIA) and HVL meconium-stained in the body (HVL-MEC-B) of PRRSV-infected dams. The expression of claudin (CLDN) 1, 3, 4, 5, 6, 7, 10, tight junction protein 1 (TJP1) and occludin (OCLN) genes were evaluated by PCR. There were no significant group differences between IUGR and N-IUGR groups, regardless of infection status, that explained the resilience of IUGR fetuses. Regarding disease progression, elevated CLDN3 was observed in END of UNIF, CLDN6 expression was lower in PLC when the fetus became infected (HVL-VIA), and CLDN10 elevated in PLC in fetuses showing evidence of compromise (HVL-MEC-B). Lastly, OCLN gene expression was higher in the END and PLC following maternal infection. In conclusion, differences in TJ integrity were mainly observed following PRRSV-2 infection with stepwise changes corresponding with disease progression.
了解与正常胎儿相比，宫内生长受限（IUGR）胎儿为何对经胎盘感染的猪繁殖与呼吸综合征病毒2型（PRRSV-2）更具抵抗力，可能会带来控制猪繁殖与呼吸综合征的其他方法。我们的目的是比较i）IUGR胎儿与非IUGR胎儿，以及ii）PRRSV-2感染后疾病进展不同表型的子宫内膜（END）和胎盘（PLC）中紧密连接蛋白子集的基因表达。在实验1中，从一项大型攻毒试验中，策略性地选取了未感染对照母畜（CTRL）所产胎儿以及高病毒载量存活（HVL-VIA）胎儿的速冻END和PLC，两组又根据脑:肝重量比进一步分为IUGR或非（N）-IUGR。在实验2中，从PRRSV感染母畜的CTRL、未感染胸腺（UNIF）、（HVL-VIA）和体内有胎粪染色的高病毒载量（HVL-MEC-B）中随机选取类似组织。通过PCR评估紧密连接蛋白（CLDN）1、3、4、5、6、7、10、紧密连接蛋白1（TJP1）和闭合蛋白（OCLN）基因的表达。无论感染状态如何，IUGR组和N-IUGR组之间均无显著组间差异，这可以解释IUGR胎儿的抵抗力。关于疾病进展，在UNIF的END中观察到CLDN3升高，胎儿感染时（HVL-VIA）PLC中的CLDN6表达较低，而在显示有受损迹象的胎儿的PLC中（HVL-MEC-B）CLDN10升高。最后，母体感染后END和PLC中的OCLN基因表达较高。总之，主要在PRRSV-2感染后观察到紧密连接完整性的差异，且这些差异随疾病进展呈逐步变化。
