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小鼠母体牙源性感染会导致后代认知能力下降。

Mouse maternal odontogenic infection with induces cognitive decline in offspring.

作者信息

Ishida Eri, Furusho Hisako, Renn Ting-Yi, Shiba Fumie, Chang Hung-Ming, Oue Hiroshi, Terayama Ryuji, Ago Yukio, Tsuga Kazuhiro, Miyauchi Mutsumi

机构信息

Department of Advanced Prosthodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

出版信息

Front Pediatr. 2023 Aug 11;11:1203894. doi: 10.3389/fped.2023.1203894. eCollection 2023.

DOI:10.3389/fped.2023.1203894
PMID:37635786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10450928/
Abstract

INTRODUCTION

(), a major periodontal pathogen, causes intrauterine infection/inflammation. Offspring exposed to intrauterine infection/inflammation have an increased risk of neurological disorders, regardless of gestational age. However, the relationship between maternal periodontitis and offspring functional/histological changes in the brain has not yet been elucidated.

METHODS

In this study, we used a gestational mouse model to investigate the effects of maternal odontogenic infection of on offspring behavior and brain tissue.

RESULTS

The step-through passive avoidance test showed that the latency of the acquisition trial was significantly shorter in the group ( < 0.05), but no difference in spontaneous motor/exploratory parameters by open-field test. was diffusely distributed throughout the brain, especially in the hippocampus. In the hippocampus and amygdala, the numbers of neuron cells and cyclic adenosine monophosphate response element binding protein-positive cells were significantly reduced (< 0.05), whereas the number of ionized calcium binding adapter protein 1-positive microglia was significantly increased (< 0.05). In the hippocampus, the number of glial fibrillary acidic protein-positive astrocytes was also significantly increased (< 0.05).

DISCUSSION

The offspring of -infected mothers have reduced cognitive function. Neurodegeneration/neuroinflammation in the hippocampus and amygdala may be caused by infection, which is maternally transmitted. The importance of eliminating maternal -odontogenic infection before or during gestation in maintenance healthy brain function in offspring should be addressed in near future.

摘要

引言

()是一种主要的牙周病原体,可导致宫内感染/炎症。暴露于宫内感染/炎症的后代患神经疾病的风险增加,与胎龄无关。然而,母亲牙周炎与后代大脑功能/组织学变化之间的关系尚未阐明。

方法

在本研究中,我们使用妊娠小鼠模型来研究母体牙源性感染()对后代行为和脑组织的影响。

结果

穿梭箱被动回避试验表明,()组习得试验的潜伏期显著缩短(<0.05),但旷场试验中自发运动/探索参数无差异。()在整个大脑中广泛分布,尤其是在海马体中。在海马体和杏仁核中,神经元细胞和环磷酸腺苷反应元件结合蛋白阳性细胞的数量显著减少(<0.05),而离子钙结合衔接蛋白1阳性小胶质细胞的数量显著增加(<0.05)。在海马体中,胶质纤维酸性蛋白阳性星形胶质细胞的数量也显著增加(<0.05)。

讨论

感染()的母亲的后代认知功能降低。海马体和杏仁核中的神经退行性变/神经炎症可能由()感染引起,这种感染是通过母体传播的。在不久的将来,应该关注在妊娠前或妊娠期间消除母体牙源性()感染对维持后代健康脑功能的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/519c03e9a3fd/fped-11-1203894-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/f929df56d11a/fped-11-1203894-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/d53ef8b2f3ec/fped-11-1203894-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/3786d2b1aefd/fped-11-1203894-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/2827efff0b3e/fped-11-1203894-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/3d657cb704e0/fped-11-1203894-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/519c03e9a3fd/fped-11-1203894-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/f929df56d11a/fped-11-1203894-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/d53ef8b2f3ec/fped-11-1203894-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/3786d2b1aefd/fped-11-1203894-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/2827efff0b3e/fped-11-1203894-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/3d657cb704e0/fped-11-1203894-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/772a/10450928/519c03e9a3fd/fped-11-1203894-g006.jpg

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