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新生儿肺炎诱导小鼠模型气道平滑肌表型异常和 AHR。

Neonatal Pneumonia Induces an Aberrant Airway Smooth Muscle Phenotype and AHR in Mice Model.

机构信息

Key Laboratory of Pediatrics in Chongqing, China.

Department of Children's Hospital of Chongqing Medical University of Education, Key Laboratory of Child Development and Disorders, China.

出版信息

Biomed Res Int. 2019 Jan 6;2019:1948519. doi: 10.1155/2019/1948519. eCollection 2019.

DOI:10.1155/2019/1948519
PMID:30723734
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6339730/
Abstract

Our previous study showed that neonatal infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the strain D39. Five weeks after infection, the lungs were collected to assess the levels of -SMA and the contractile proteins of ASM. Our results indicate that neonatal pneumonia significantly increased adulthood lung -SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.

摘要

我们之前的研究表明，新生儿感染会加重卵清蛋白诱导的过敏性哮喘模型中的气道炎症和气道高反应性（AHR）。由于气道平滑肌（ASM）在 AHR 发展中起着关键作用，我们旨在研究新生儿肺炎对 ASM 结构和 AHR 发展的影响。通过鼻腔感染 1 周龄 BALB/C 小鼠 D39 株来建立非致死性新生儿肺炎。感染后 5 周，收集肺部评估 -SMA 和 ASM 的收缩蛋白水平。我们的结果表明，新生儿肺炎显著增加了成年肺部 -SMA 和 SMMHC 蛋白的产生，并加重了气道炎症细胞浸润和细胞因子释放。此外，与未感染对照组相比，新生儿肺炎组的 Penh 值显著更高。这些数据表明，新生儿肺炎促进了小鼠模型中异常的 ASM 表型和 AHR 发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/345773ae1119/BMRI2019-1948519.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/7c9c85627f7e/BMRI2019-1948519.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/2b79273e041e/BMRI2019-1948519.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/c19c0ad34717/BMRI2019-1948519.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/345773ae1119/BMRI2019-1948519.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/7c9c85627f7e/BMRI2019-1948519.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/2b79273e041e/BMRI2019-1948519.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/c19c0ad34717/BMRI2019-1948519.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd5/6339730/345773ae1119/BMRI2019-1948519.004.jpg

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Th17/IL-17 Axis Regulated by Airway Microbes Get Involved in the Development of Asthma.气道微生物调控的 Th17/IL-17 轴参与哮喘的发病机制。
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