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Stem Cells and COVID-19 干细胞与COVID-19
IF 0.7 Q4 RESPIRATORY SYSTEM Pub Date : 2020-01-01 DOI: 10.1016/c2020-0-03301-3
A. Antoniadis, Rousana Pechlivanidou, E. Bouros, Demosthenes Bouros
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引用次数: 2
Effect of low doses of lipopolysaccharide prior to ozone exposure on bronchoalveolar lavage: Differences between wild type and surfactant protein A-deficient mice. 臭氧暴露前低剂量脂多糖对支气管肺泡灌洗的影响:野生型和表面活性剂蛋白a缺陷小鼠的差异
IF 0.5 Q4 RESPIRATORY SYSTEM Pub Date : 2009-01-01
Rizwanul Haque, Todd M Umstead, Kwangmi Ahn, David S Phelps, Joanna Floros

BACKGROUND: Several aspects of the inflammatory response to a single insult, i.e., exposure to 2 ppm of ozone (O(3)) for 3 h or 6 h, are less pronounced in surfactant protein A deficient (SP-A -/-) mice (KO) than in wild type mice (WT). It was hypothesized that a mild insult, specifically low doses of lipopolysaccharide (LPS), would adversely affect host defense and differentially potentiate O(3)-induced injury in WT and KO mice. METHODS: WT and KO mice were treated with different doses of LPS or LPS (2 ng) + O(3) (2 ppm) or filtered air (FA) for 3 h, then sacrificed 4 h following exposure (O(3), FA) or 20 h after LPS treatment alone. Several endpoints of inflammation were measured in bronchoalveolar lavage (BAL). RESULTS: 1) At 20 h after LPS treatment alone, both WT and KO mice exhibited signs of inflammation, but with differences in the macrophage inflammatory protein 2 (MIP-2) response pattern, total cells (at 0.5 ng LPS) and basal levels of oxidized protein and phospholipids; 2) After LPS + O(3), KO compared to WT showed decrease in polymorphonuclear leukocytes (PMNs) and MIP-2 and increase in phospholipids, and after LPS + FA an increase in total cells; 3) WT after LPS + FA showed an increase in SP-A with no further increase after LPS + O(3), and an increase in oxidized SP-A dimer following O(3) or LPS + O(3). CONCLUSIONS: LPS treatment has negative effects on inflammation endpoints in mouse BAL long after exposure and renders KO mice less capable of responding to a second insult. LPS and O(3) affect SP-A, quantitatively and qualitatively, respectively.

背景:对单一损伤,即暴露于2 ppm臭氧(O(3)) 3小时或6小时的炎症反应的几个方面,表面活性剂蛋白a缺陷(SP-A -/-)小鼠(KO)比野生型小鼠(WT)更不明显。据推测,轻微的损伤,特别是低剂量的脂多糖(LPS),会对WT和KO小鼠的宿主防御产生不利影响,并不同程度地增强O(3)诱导的损伤。方法:将WT和KO小鼠分别用不同剂量的LPS或LPS (2 ng) + O(3) (2 ppm)或过滤空气(FA)处理3 h,然后在暴露(O(3), FA)后4 h或单独LPS处理20 h后处死。在支气管肺泡灌洗(BAL)中测量炎症的几个终点。结果:1)单独LPS处理20 h后,WT和KO小鼠均出现炎症迹象,但巨噬细胞炎症蛋白2 (MIP-2)反应模式、总细胞(0.5 ng LPS)和氧化蛋白和磷脂基础水平存在差异;2) LPS + O(3)后,KO与WT相比,多形核白细胞(PMNs)和MIP-2减少,磷脂增加,LPS + FA后总细胞增加;3) LPS + FA处理后的WT中SP-A增加,LPS + O(3)处理后SP-A氧化二聚体增加,而LPS + O(3)处理后SP-A氧化二聚体增加。结论:LPS治疗在暴露后很长时间内对小鼠BAL的炎症终点有负面影响,并使KO小鼠对第二次损伤的反应能力降低。LPS和O(3)分别定量和定性地影响SP-A。
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引用次数: 0
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Pneumon
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