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在感染李斯特菌的 10-14 天孕鼠的胎儿组织中,细菌负荷和炎症与 IL-17a 或 IL-22 无关。

Bacterial load and inflammation in fetal tissues is not dependent on IL-17a or IL-22 in 10-14 day pregnant mice infected with Listeria monocytogenes.

机构信息

Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University, 700 SW 30th Street, Corvallis, OR 97331, USA.

出版信息

Microb Pathog. 2013 Mar;56:47-52. doi: 10.1016/j.micpath.2012.11.003. Epub 2012 Nov 20.

DOI:10.1016/j.micpath.2012.11.003
PMID:23178254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3578105/
Abstract

In this study, we first assessed the effect of intragastric infection of pregnant mice with Listeria monocytogenes on relative expression of select genes associated with T cell subsets. Relative gene expression was moderately increased in placental tissues for IFNγ, IL-4, IL-17a, IL-22, CD3, and FoxP3. To assess the roles of IL-17a and IL-22 in resistance to listeriosis during pregnancy, we compared the severity of maternal and fetal infection in IL-17a((-/-)), IL-22((-/-)), and IL-17a((-/-))/IL-22((-/-)) mice with that of wild type C57BL/6 mice. Intragastric infection with modest numbers of bacterial cells (10(5) CFU) caused reproducible maternal and fetal infection in all four mouse strains. We recovered greater numbers of CFU from the bloodstream of pregnant IL-22((-/-)) mice than pregnant wild type mice. Otherwise we found no significant difference in bacterial load in maternal or fetal tissues (spleen, liver, fetoplacental units) from pregnant IL-17a((-/-)), IL-22((-/-)), or IL-17a((-/-))/IL-22((-/-)) or wild type mice. Nor did we observe histopathologic differences in severity of inflammation in maternal or fetal tissues from the various groups of mice. Although IL-17a and IL-22 are up-regulated in placental tissue, our study suggests that antibacterial resistance and the host inflammatory response are not dependent on IL-17a or IL-22 during infection of mice with L. monocytogenes at 10-14 days of gestation.

摘要

在这项研究中,我们首先评估了李斯特菌感染妊娠小鼠的胃内感染对与 T 细胞亚群相关的选择基因的相对表达的影响。IFNγ、IL-4、IL-17a、IL-22、CD3 和 FoxP3 在胎盘组织中的相对基因表达适度增加。为了评估 IL-17a 和 IL-22 在妊娠期间李斯特菌感染抗性中的作用,我们比较了 IL-17a((-/-))、IL-22((-/-))和 IL-17a((-/-))/IL-22((-/-))小鼠与野生型 C57BL/6 小鼠的母体和胎儿感染的严重程度。用适度数量的细菌细胞(10(5) CFU)进行胃内感染,在所有四种小鼠品系中均能重现母体和胎儿感染。我们从妊娠 IL-22((-/-))小鼠的血液中回收了比妊娠野生型小鼠更多的 CFU。否则,我们在母体或胎儿组织(脾、肝、胎胎盘单位)中未发现来自妊娠 IL-17a((-/-))、IL-22((-/-))或 IL-17a((-/-))/IL-22((-/-))或野生型小鼠的细菌负荷有任何显著差异。我们也没有观察到来自各种小鼠组的母体或胎儿组织中炎症严重程度的组织病理学差异。尽管 IL-17a 和 IL-22 在胎盘组织中上调,但我们的研究表明,在妊娠 10-14 天感染李斯特菌时,抗菌抗性和宿主炎症反应不依赖于 IL-17a 或 IL-22。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/f6ef43f856a4/nihms-422791-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/12868f28c3be/nihms-422791-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/e5dcee728077/nihms-422791-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/f6ef43f856a4/nihms-422791-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/12868f28c3be/nihms-422791-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/e5dcee728077/nihms-422791-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/974b/3578105/f6ef43f856a4/nihms-422791-f0003.jpg

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