Molecular Food Microbiology Laboratory, Department of Food Science, Purdue University, West Lafayette, IN, 47907, USA.
Department of Comparative Pathobiology, Purdue University, West Lafayette, IN, 47907, USA.
Microb Pathog. 2021 Feb;151:104752. doi: 10.1016/j.micpath.2021.104752. Epub 2021 Jan 21.
Pregnancy is a high-risk factor for foodborne pathogen Listeria monocytogenes (Lm), which causes abortion, premature birth, or stillbirth. The primary route of Lm transmission is oral hence intestinal epithelial barrier crossing is a prerequisite for systemic spread. Intestinal barrier crossing, in part, is attributed to the interaction of Listeria adhesion protein (LAP) with its cognate receptor, Hsp60. In a recent study, we showed that oral-dosing of bioengineered Lactobacillus caseiprobiotic (BLP) expressing the LAP protected nonpregnant mice from lethal infection; however, its ability to prevent listeriosis during pregnancy is not known. Therefore, we investigated whether BLP could prevent fetoplacental transmission of Lm in a pregnant guinea pig model. After 14 consecutive days on probiotic (~10 CFU/ml in drinking water), pregnant guinea pigs (gestational days 24-28) were orally challenged with Lm (9 × 10-2.5 × 10 CFU/animal) and were euthanized 72 h post-infection. Maternal mesenteric lymph node (MLN), liver, spleen, lungs, blood, and placenta, and fetal liver were analyzed for the presence/absence of Lm. All tissues/organs from Lm-challenged naïve dams and fetuses were Lm positive. Similar tissue distribution was also seen in guinea pigs that received wild-type Lactobacillus casei (LbcWT). Remarkably, Lm was absent in the maternal blood, kidney, lungs, and placenta, and fetal liver from the BLP-fed group even though the Lm was present in the maternal liver, spleen, and MLN. BLP feeding also suppressed Lm-induced inflammatory response in mothers. These data highlight the potential for the prevention of fetoplacental transmission of Lm by LAP-expressing BLP during pregnancy.
妊娠是食源性病原体单核细胞增生李斯特菌(Lm)的高危因素,可导致流产、早产或死产。Lm 的主要传播途径是经口,因此肠道上皮屏障的穿越是系统传播的前提。部分原因是李斯特菌黏附蛋白(LAP)与其同源受体 Hsp60 的相互作用。在最近的一项研究中,我们表明,口服表达 LAP 的工程化乳杆菌酪蛋白益生菌(BLP)可保护非妊娠小鼠免受致死性感染;然而,其在妊娠期间预防李斯特菌病的能力尚不清楚。因此,我们研究了 BLP 是否可以预防怀孕豚鼠模型中的胎-胎盘李斯特菌传播。在连续 14 天口服益生菌(饮用水中约 10 CFU/ml)后,怀孕豚鼠(妊娠第 24-28 天)经口接受 Lm(9×10-2.5×10 CFU/动物)挑战,并在感染后 72 小时安乐死。分析母体肠系膜淋巴结(MLN)、肝、脾、肺、血和胎盘以及胎肝中 Lm 的存在/缺失情况。Lm 挑战的初产母体和胎儿的所有组织/器官均为 Lm 阳性。接受野生型乳杆菌酪蛋白(LbcWT)的豚鼠也出现了类似的组织分布。值得注意的是,即使在母体肝、脾和 MLN 中存在 Lm,BLP 喂养组的母血、肾、肺和胎盘以及胎肝中均未见 Lm。BLP 喂养还抑制了 Lm 诱导的母体炎症反应。这些数据突出了 LAP 表达的 BLP 在怀孕期间预防 Lm 胎-胎盘传播的潜力。