母体甲状腺功能亢进改变大鼠蜕膜中免疫介质的分布和自然杀伤细胞的数量

IF 2.3 4区 生物学 Q4 CELL BIOLOGY
Luciano Cardoso Santos , Cíntia Almeida de Souza , Juneo Freitas Silva , Natália Melo Ocarino , Rogéria Serakides
{"title":"母体甲状腺功能亢进改变大鼠蜕膜中免疫介质的分布和自然杀伤细胞的数量","authors":"Luciano Cardoso Santos ,&nbsp;Cíntia Almeida de Souza ,&nbsp;Juneo Freitas Silva ,&nbsp;Natália Melo Ocarino ,&nbsp;Rogéria Serakides","doi":"10.1016/j.acthis.2023.152026","DOIUrl":null,"url":null,"abstract":"<div><p><span>Decidual immunological mediators modulate placental formation, decidualization<span><span> and fetal development. However, the effect of maternal </span>hyperthyroidism<span><span><span> on decidual immunology needs further research. The aim of this study was to evaluate the population of uterine </span>natural killer cells<span> (uNKs) and the expression of immunological mediators in the decidua of female rats throughout pregnancy. </span></span>Wistar rats were used and hyperthyroidism was induced by daily administration of </span></span></span><span>L</span><span><span>-thyroxine (T4) throughout pregnancy. The population of uNK cells in decidua was evaluated by immunostaining<span> Lectin DBA, as well as the expression of </span></span>interferon γ<span><span><span> (INFγ), macrophage migration inhibitory factor (MIF), </span>interleukin 15<span> (IL-15) and inducible nitric oxide synthase (iNOS) at 7, 10, 12, 14 and 19 days of gestation (DG). Maternal hyperthyroidism reduced the DBA+ uNK cell population in the decidua at 7 (P &lt; 0.05) and 10 (P &lt; 0.01) DGs compared to that in the control group, while it increased in the basal decidua (P &lt; 0.05) and </span></span>metrial gland<span> (P &lt; 0.0001) at the 12th DG. Hyperthyroidism also increased immunostaining of IL-15 (P &lt; 0.0001), INFγ (P &lt; 0.05), and MIF (P &lt; 0.05) in the 7th DG, and increased immunostaining of IL-15 (P &lt; 0.0001) and MIF (P &lt; 0.01) in </span></span></span><sup>th</sup><span><span>e 10th DG. However, excess thyroxine reduced IL-15 expression in the metrial gland and/or basal decidua in the 12th (P &lt; 0.05), 14th (P &lt; 0.01), and 19th (P &lt; 0.001) DGs, as was also observed for INFγ in the basal decidua (P&lt;0.001) and metrial gland (P &lt; 0.0001) in the 12th DG. Regarding iNOS, an antiinflammatory cytokine, lower expression was observed in the basal decidua of hyperthyroid animals at 7 and 12 DGs (P &lt; 0.05), whereas an increase occurred in the 10th DG (P &lt; 0.05). These data demonstrate that maternal hyperthyroidism in female rats, particularly between 7 and 10 DGs, reduces the population of DBA+ uNKs in the decidua and increases the expression of inflammatory cytokines, suggesting a more proinflammatory environment in </span>early pregnancy caused by this gestational disease.</span></p></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":null,"pages":null},"PeriodicalIF":2.3000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Maternal hyperthyroidism alters the immunological mediators profile and population of natural killers cells in decidua of rats\",\"authors\":\"Luciano Cardoso Santos ,&nbsp;Cíntia Almeida de Souza ,&nbsp;Juneo Freitas Silva ,&nbsp;Natália Melo Ocarino ,&nbsp;Rogéria Serakides\",\"doi\":\"10.1016/j.acthis.2023.152026\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span>Decidual immunological mediators modulate placental formation, decidualization<span><span> and fetal development. However, the effect of maternal </span>hyperthyroidism<span><span><span> on decidual immunology needs further research. The aim of this study was to evaluate the population of uterine </span>natural killer cells<span> (uNKs) and the expression of immunological mediators in the decidua of female rats throughout pregnancy. </span></span>Wistar rats were used and hyperthyroidism was induced by daily administration of </span></span></span><span>L</span><span><span>-thyroxine (T4) throughout pregnancy. The population of uNK cells in decidua was evaluated by immunostaining<span> Lectin DBA, as well as the expression of </span></span>interferon γ<span><span><span> (INFγ), macrophage migration inhibitory factor (MIF), </span>interleukin 15<span> (IL-15) and inducible nitric oxide synthase (iNOS) at 7, 10, 12, 14 and 19 days of gestation (DG). Maternal hyperthyroidism reduced the DBA+ uNK cell population in the decidua at 7 (P &lt; 0.05) and 10 (P &lt; 0.01) DGs compared to that in the control group, while it increased in the basal decidua (P &lt; 0.05) and </span></span>metrial gland<span> (P &lt; 0.0001) at the 12th DG. Hyperthyroidism also increased immunostaining of IL-15 (P &lt; 0.0001), INFγ (P &lt; 0.05), and MIF (P &lt; 0.05) in the 7th DG, and increased immunostaining of IL-15 (P &lt; 0.0001) and MIF (P &lt; 0.01) in </span></span></span><sup>th</sup><span><span>e 10th DG. However, excess thyroxine reduced IL-15 expression in the metrial gland and/or basal decidua in the 12th (P &lt; 0.05), 14th (P &lt; 0.01), and 19th (P &lt; 0.001) DGs, as was also observed for INFγ in the basal decidua (P&lt;0.001) and metrial gland (P &lt; 0.0001) in the 12th DG. Regarding iNOS, an antiinflammatory cytokine, lower expression was observed in the basal decidua of hyperthyroid animals at 7 and 12 DGs (P &lt; 0.05), whereas an increase occurred in the 10th DG (P &lt; 0.05). These data demonstrate that maternal hyperthyroidism in female rats, particularly between 7 and 10 DGs, reduces the population of DBA+ uNKs in the decidua and increases the expression of inflammatory cytokines, suggesting a more proinflammatory environment in </span>early pregnancy caused by this gestational disease.</span></p></div>\",\"PeriodicalId\":6961,\"journal\":{\"name\":\"Acta histochemica\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta histochemica\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0065128123000326\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta histochemica","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0065128123000326","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 1

摘要

蜕膜免疫介质调节胎盘形成、蜕膜化和胎儿发育。然而,母体甲状腺功能亢进对蜕膜免疫学的影响还有待进一步研究。本研究的目的是评估妊娠期雌性大鼠蜕膜中子宫自然杀伤细胞(uNKs)的数量和免疫介质的表达。使用Wistar大鼠,通过在整个妊娠期间每天给予L-甲状腺素(T4)来诱导甲状腺功能亢进。通过免疫染色Lectin DBA,以及干扰素γ(INFγ)、巨噬细胞迁移抑制因子(MIF)、白细胞介素15(IL-15)和诱导型一氧化氮合酶(iNOS)在妊娠7、10、12、14和19天的表达来评估蜕膜中的uNK细胞群。与对照组相比,母体甲状腺功能亢进在7(P<;0.05)和10(P<)DG时降低了蜕膜中的DBA+uNK细胞群,而在第12 DG时增加了基底蜕膜(P<!0.05)和子宫腺(P<:0.0001)。甲状腺功能亢进还增加了第7个DG中IL-15(P<;0.0001)、INFγ(P<!0.05)和MIF(P>;0.05)的免疫染色,并增加了第10个DG中的IL-15(P/lt!0.0001)和MIF的免疫染色。然而,过量的甲状腺素降低了第12个(P<;0.05)、第14个(P>;0.01)和第19个(P&<;0.001)DG的子宫腺和/或基底蜕膜中IL-15的表达,在第12个DG的基底蜕膜(P<)和子宫腺(P<!0.0001)中也观察到了INFγ的表达。关于iNOS,一种抗炎细胞因子,在7和12 DG时,在甲状腺功能亢进动物的基底蜕膜中观察到较低的表达(P<;0.05),而在第10 DG中出现增加(P<)。这些数据表明,雌性大鼠的母体甲状腺功能亢进,特别是在7和10 DG之间,减少了蜕膜中DBA+uNKs的数量,并增加了炎性细胞因子的表达,这表明这种妊娠期疾病在妊娠早期会产生更大的促炎环境。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Maternal hyperthyroidism alters the immunological mediators profile and population of natural killers cells in decidua of rats

Decidual immunological mediators modulate placental formation, decidualization and fetal development. However, the effect of maternal hyperthyroidism on decidual immunology needs further research. The aim of this study was to evaluate the population of uterine natural killer cells (uNKs) and the expression of immunological mediators in the decidua of female rats throughout pregnancy. Wistar rats were used and hyperthyroidism was induced by daily administration of L-thyroxine (T4) throughout pregnancy. The population of uNK cells in decidua was evaluated by immunostaining Lectin DBA, as well as the expression of interferon γ (INFγ), macrophage migration inhibitory factor (MIF), interleukin 15 (IL-15) and inducible nitric oxide synthase (iNOS) at 7, 10, 12, 14 and 19 days of gestation (DG). Maternal hyperthyroidism reduced the DBA+ uNK cell population in the decidua at 7 (P < 0.05) and 10 (P < 0.01) DGs compared to that in the control group, while it increased in the basal decidua (P < 0.05) and metrial gland (P < 0.0001) at the 12th DG. Hyperthyroidism also increased immunostaining of IL-15 (P < 0.0001), INFγ (P < 0.05), and MIF (P < 0.05) in the 7th DG, and increased immunostaining of IL-15 (P < 0.0001) and MIF (P < 0.01) in the 10th DG. However, excess thyroxine reduced IL-15 expression in the metrial gland and/or basal decidua in the 12th (P < 0.05), 14th (P < 0.01), and 19th (P < 0.001) DGs, as was also observed for INFγ in the basal decidua (P<0.001) and metrial gland (P < 0.0001) in the 12th DG. Regarding iNOS, an antiinflammatory cytokine, lower expression was observed in the basal decidua of hyperthyroid animals at 7 and 12 DGs (P < 0.05), whereas an increase occurred in the 10th DG (P < 0.05). These data demonstrate that maternal hyperthyroidism in female rats, particularly between 7 and 10 DGs, reduces the population of DBA+ uNKs in the decidua and increases the expression of inflammatory cytokines, suggesting a more proinflammatory environment in early pregnancy caused by this gestational disease.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Acta histochemica
Acta histochemica 生物-细胞生物学
CiteScore
4.60
自引率
4.00%
发文量
107
审稿时长
23 days
期刊介绍: Acta histochemica, a journal of structural biochemistry of cells and tissues, publishes original research articles, short communications, reviews, letters to the editor, meeting reports and abstracts of meetings. The aim of the journal is to provide a forum for the cytochemical and histochemical research community in the life sciences, including cell biology, biotechnology, neurobiology, immunobiology, pathology, pharmacology, botany, zoology and environmental and toxicological research. The journal focuses on new developments in cytochemistry and histochemistry and their applications. Manuscripts reporting on studies of living cells and tissues are particularly welcome. Understanding the complexity of cells and tissues, i.e. their biocomplexity and biodiversity, is a major goal of the journal and reports on this topic are especially encouraged. Original research articles, short communications and reviews that report on new developments in cytochemistry and histochemistry are welcomed, especially when molecular biology is combined with the use of advanced microscopical techniques including image analysis and cytometry. Letters to the editor should comment or interpret previously published articles in the journal to trigger scientific discussions. Meeting reports are considered to be very important publications in the journal because they are excellent opportunities to present state-of-the-art overviews of fields in research where the developments are fast and hard to follow. Authors of meeting reports should consult the editors before writing a report. The editorial policy of the editors and the editorial board is rapid publication. Once a manuscript is received by one of the editors, an editorial decision about acceptance, revision or rejection will be taken within a month. It is the aim of the publishers to have a manuscript published within three months after the manuscript has been accepted
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信