• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

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

内毒素对新生大鼠肺部的影响:炎症反应的年龄依赖性损伤

Effects of endotoxin in the lungs of neonatal rats: age-dependent impairment of the inflammatory response.

作者信息

Martin T R, Ruzinski J T, Wilson C B, Skerrett S J

机构信息

Medical Research Service, Seattle VA Medical Center, WA 98108.

出版信息

J Infect Dis. 1995 Jan;171(1):134-44. doi: 10.1093/infdis/171.1.134.

DOI:10.1093/infdis/171.1.134
PMID:7798654
Abstract

Age-dependent maturation of the intrapulmonary inflammatory responses to bacterial lipopolysaccharide (LPS) was studied because nosocomial gram-negative infections cause morbidity in newborn infants. Escherichia coli LPS or live E. coli were injected into the airways of neonatal or adult rats; intrapulmonary recruitment of leukocytes was measured 6 h later. Neonates showed age- and dose-dependent impairment of intrapulmonary neutrophil recruitment after intratracheal administration of LPS or live E. coli that persisted for the first 28 days of life. Neonatal and adult alveolar macrophages released similar amounts of neutrophil chemotactic activity and tumor necrosis factor in response to incubation with LPS in vitro. Treatment of neonates with intratracheal or systemic interferon-gamma did not augment the response to LPS. Thus, intrapulmonary inflammatory responses to LPS and gram-negative bacteria are impaired early in life and do not approach adult levels until approximately 4 weeks of age.

摘要

由于医院获得性革兰氏阴性菌感染会导致新生儿发病,因此研究了肺部对细菌脂多糖(LPS)的炎症反应随年龄的成熟情况。将大肠杆菌LPS或活的大肠杆菌注入新生大鼠或成年大鼠的气道;6小时后测量肺内白细胞募集情况。新生大鼠在气管内给予LPS或活的大肠杆菌后,肺内中性粒细胞募集出现年龄和剂量依赖性损害,这种损害在出生后的前28天持续存在。新生和成年肺泡巨噬细胞在体外与LPS孵育后释放的中性粒细胞趋化活性和肿瘤坏死因子量相似。气管内或全身给予新生儿干扰素-γ并不能增强对LPS的反应。因此,肺部对LPS和革兰氏阴性菌的炎症反应在生命早期受损,直到大约4周龄时才接近成年水平。

相似文献

1
Effects of endotoxin in the lungs of neonatal rats: age-dependent impairment of the inflammatory response.内毒素对新生大鼠肺部的影响:炎症反应的年龄依赖性损伤
J Infect Dis. 1995 Jan;171(1):134-44. doi: 10.1093/infdis/171.1.134.
2
Acute ethanol intoxication suppresses the pulmonary inflammatory response in rats challenged with intrapulmonary endotoxin.急性乙醇中毒可抑制经肺内注射内毒素攻击的大鼠的肺部炎症反应。
Alcohol Clin Exp Res. 1997 Aug;21(5):773-8.
3
Inhibition of pulmonary neutrophil trafficking during endotoxemia is dependent on the stimulus for migration.内毒素血症期间肺中性粒细胞迁移的抑制取决于迁移刺激因素。
Am J Respir Cell Mol Biol. 1999 Apr;20(4):769-76. doi: 10.1165/ajrcmb.20.4.3481.
4
Hypothermia inhibits cytokine release of alveolar macrophage and activation of nuclear factor kappaB in endotoxemic lung.体温过低会抑制内毒素血症肺中肺泡巨噬细胞的细胞因子释放以及核因子κB的激活。
Intensive Care Med. 2004 Aug;30(8):1638-44. doi: 10.1007/s00134-004-2336-z. Epub 2004 May 28.
5
Interferon-gamma enhances the pulmonary CXC chemokine response to intratracheal lipopolysaccharide challenge.干扰素-γ增强肺部对气管内脂多糖攻击的CXC趋化因子反应。
J Infect Dis. 2003 Jan 1;187(1):62-9. doi: 10.1086/346027. Epub 2002 Dec 13.
6
Lipopolysaccharide (LPS) inhalation in healthy subjects increases neutrophils, lymphocytes and fibronectin levels in bronchoalveolar lavage fluid.健康受试者吸入脂多糖(LPS)会增加支气管肺泡灌洗液中的中性粒细胞、淋巴细胞和纤连蛋白水平。
Eur Respir J. 1992 Sep;5(8):992-6.
7
Regulation of nitric oxide release by macrophages after intratracheal lipopolysaccharide.气管内注入脂多糖后巨噬细胞对一氧化氮释放的调节
Am J Respir Cell Mol Biol. 1995 Jul;13(1):45-53. doi: 10.1165/ajrcmb.13.1.7541222.
8
Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA.内源性 MCP-1 促进 LPS 和 LTA 诱导的肺部炎症。
Mol Immunol. 2011 Jul;48(12-13):1468-76. doi: 10.1016/j.molimm.2011.04.001. Epub 2011 May 6.
9
Antibody-mediated depletion of tumor necrosis factor-alpha impairs pulmonary host defenses to Legionella pneumophila.抗体介导的肿瘤坏死因子-α耗竭会损害肺部对嗜肺军团菌的宿主防御能力。
J Infect Dis. 1997 Oct;176(4):1019-28. doi: 10.1086/516530.
10
In vivo effect of surfactant on inflammatory cytokines during endotoxin-induced lung injury in rodents.在脂多糖诱导的啮齿动物肺损伤中,表面活性剂对炎症细胞因子的体内作用。
J Immunotoxicol. 2011 Oct-Dec;8(4):274-83. doi: 10.3109/1547691X.2011.591294. Epub 2011 Jul 18.

引用本文的文献

1
Age-dependent differences in pulmonary host responses in ARDS: a prospective observational cohort study.急性呼吸窘迫综合征中肺部宿主反应的年龄依赖性差异:一项前瞻性观察队列研究。
Ann Intensive Care. 2019 May 14;9(1):55. doi: 10.1186/s13613-019-0529-4.
2
Innate Immunity to Respiratory Infection in Early Life.生命早期对呼吸道感染的天然免疫
Front Immunol. 2017 Nov 14;8:1570. doi: 10.3389/fimmu.2017.01570. eCollection 2017.
3
The innate immune response to lower respiratory tract E. Coli infection and the role of the CCL2-CCR2 axis in neonatal mice.
对下呼吸道大肠杆菌感染的先天免疫反应及 CCL2-CCR2 轴在新生小鼠中的作用。
Cytokine. 2017 Sep;97:108-116. doi: 10.1016/j.cyto.2017.06.002. Epub 2017 Jun 16.
4
Understanding the Impact of Infection, Inflammation, and Their Persistence in the Pathogenesis of Bronchopulmonary Dysplasia.了解感染、炎症及其持续存在对支气管肺发育不良发病机制的影响。
Front Med (Lausanne). 2015 Dec 21;2:90. doi: 10.3389/fmed.2015.00090. eCollection 2015.
5
Immune response to intrapharyngeal LPS in neonatal and juvenile mice.新生和幼年小鼠对咽内脂多糖的免疫反应。
Am J Respir Cell Mol Biol. 2015 Mar;52(3):323-31. doi: 10.1165/rcmb.2014-0100OC.
6
Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia.支气管肺发育不良发病机制中的产后炎症
Birth Defects Res A Clin Mol Teratol. 2014 Mar;100(3):189-201. doi: 10.1002/bdra.23220. Epub 2014 Feb 27.
7
Attenuated mRNA expression of inflammatory mediators in neonatal rat lung following lipopolysaccharide treatment.脂多糖处理后新生大鼠肺中炎症介质的 mRNA 表达减弱。
J Inflamm Res. 2012;5:99-109. doi: 10.2147/JIR.S33737. Epub 2012 Sep 7.
8
Endotoxin inhalation alters lung development in neonatal mice.内毒素吸入可改变新生小鼠的肺发育。
Am J Ind Med. 2012 Dec;55(12):1146-58. doi: 10.1002/ajim.22061. Epub 2012 May 10.
9
Impaired neonatal macrophage phagocytosis is not explained by overproduction of prostaglandin E2.新生儿巨噬细胞吞噬功能受损不能用前列腺素 E2 产生过多来解释。
Respir Res. 2011 Dec 5;12(1):155. doi: 10.1186/1465-9921-12-155.
10
Lipopolysaccharide-induced injury is more pronounced in fetal transgenic ErbB4-deleted lungs.脂多糖诱导的损伤在胎儿转基因 ErbB4 缺失肺中更为明显。
Am J Physiol Lung Cell Mol Physiol. 2011 Oct;301(4):L490-9. doi: 10.1152/ajplung.00131.2010. Epub 2011 Jul 1.