Suppr超能文献

早产儿肺部炎症发病机制的新见解。

New insights into the pathogenesis of pulmonary inflammation in preterm infants.

作者信息

Speer C P

机构信息

University Children's Hospital, Würzburg, Germany.

出版信息

Biol Neonate. 2001;79(3-4):205-9. doi: 10.1159/000047092.

Abstract

Chronic lung disease (CLD) and bronchopulmonary dysplasia are associated with a significant inflammatory response of the airways and the interstitium of the lungs. Besides inflammatory cells, various cytokines, lipid mediators, proteolytic enzymes and toxic oxygen radicals may play an essential role in the pathogenesis of this disease. Intrauterine exposure to chorioamnionitis or proinflammatory cytokines has been shown to induce a pulmonary and systemic inflammatory response in the fetus. In this subgroup, antenatal infection may prime the lung such that minimally injurious postnatal events provoke an excessive inflammatory response in the airways and the pulmonary tissue. Inflammation and lung injury most certainly affect normal alveolization and pulmonary vascular development in preterm infants with CLD.

摘要

慢性肺部疾病(CLD)和支气管肺发育不良与气道和肺间质的显著炎症反应相关。除炎症细胞外,各种细胞因子、脂质介质、蛋白水解酶和毒性氧自由基可能在该疾病的发病机制中起重要作用。宫内暴露于绒毛膜羊膜炎或促炎细胞因子已被证明可在胎儿中诱导肺部和全身炎症反应。在这一亚组中,产前感染可能使肺部致敏,以至于产后轻微的损伤事件会在气道和肺组织中引发过度的炎症反应。炎症和肺损伤几乎肯定会影响患有CLD的早产儿的正常肺泡化和肺血管发育。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验