Inflammatory mechanisms in neonatal chronic lung disease
Inflammatory mechanisms in neonatal chronic lung disease
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新生儿慢性肺病的炎症机制
DOI：
--
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发表时间：
1999
影响因子：
3.6
通讯作者：
C. P. Speer
中科院分区：
文献类型：
--
作者：
C. P. Speer
Abstract Chronic lung disease (CLD) of preterm infants has a multifactorial aetiology. Oxygen toxicity, mechanical injury (barotrauma), volutrauma as well as prenatal and postnatal infections most likely contribute to pulmonary injury in the immature lung of preterm infants. There is sufficient evidence that respiratory distress syndrome and CLD are associated with a significant inflammatory response of the airways and the interstitium of the lungs; besides neutrophils, alveolar and interstitial macrophages immunoreactive for tumour necrosis factor-α (TNF-α) are found in large numbers. Phagocyte influx is possibly mediated by chemotactic and chemokinetic factors present in the broncho-alveolar secretions: interleukin-8, leukotriene B4, C5a, elastin fragments, macrophage-inflammatory protein-1α and other chemokines. Increased concentrations of soluble selectins and intercellular adhesion molecule-1 in broncho-alveolar secretions and the serum of infants with CLD possibly reflect neutrophil diapedesis. Lipid mediators including leukotrienes, prostacyclin, platelet activating and other mediators such as the pro-inflammatory cytokines TNF-α, interleukin-1 and -6, exert various effects on the airways and the vascular system by increasing the microvascular permeability which is one of the most important pathophysiological factors of early CLD. Pulmonary cells of preterm infants may be unable to downregulate inflammation through the expression of the anti-inflammatory cytokine interleukin-10. Inflammatory cells can cause severe lung damage by release of potent proteases (elastase), cytokines and by generation of toxic oxygen radicals (O2-, •OH). The presence of free elastase acitivity and the protease-antiprotease imbalance has been well documented. In fact, increased concentrations of products of elastolytic fibre degradation and of oxygen radical mediated lipid peroxidation were detected in infants with CLD.
Conclusion The complex interaction between mediators of inflammation and fibrosis has still to be defined. Moreover, the possible interference of inflammation with postnatal lung development especially with the alveolarization process has not been evaluated yet.
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分泌性白细胞蛋白酶抑制剂和支气管肺发育不良中的肺部炎症。
DOI：
10.1016/s0022-3476(94)70209-8
发表时间：
1994
期刊：
The Journal of pediatrics
影响因子：
--
作者：
Watterberg,KL;Carmichael,DF;Gerdes,JS;Werner,S;Backstrom,C;Murphy,S
通讯作者：
Murphy,S
影响因子：
8
作者：
K. Watterberg;L. Demers;S. Scott;S. Murphy
通讯作者：
K. Watterberg;L. Demers;S. Scott;S. Murphy
暴露于蛋白水解酶的单核细胞源性巨噬细胞增强氧代谢物的释放：中性粒细胞弹性蛋白酶和组织蛋白酶 G 的活性。
DOI：
--
发表时间：
1984
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Speer,CP;Pabst,MJ;Hedegaard,HB;Rest,RF;JohnstonJr,RB
通讯作者：
JohnstonJr,RB
患有细菌性肺部感染的儿童的支气管肺泡洗液中白细胞介素 1 的水平升高。
DOI：
10.1164/ajrccm/142.2.365
发表时间：
1990
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Wilmott,RW;Kassab,JT;Kilian,PL;Benjamin,WR;Douglas,SD;Wood,RE
通讯作者：
Wood,RE
支气管肺发育不良的支气管肺泡炎症病理生理学。
影响因子：
2.1
作者：
Zimmerman,JJ
通讯作者：
Zimmerman,JJ