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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Brain trauma leads to enhanced lung inflammation and injury: evidence for role of P4504Fs in resolution.
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Brain trauma leads to enhanced lung inflammation and injury: evidence for role of P4504Fs in resolution.

机译：脑外伤导致肺部炎症和损伤加剧：P4504Fs在分解中的作用证据。

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摘要

Traumatic brain injury is known to cause several secondary effects, which lead to multiple organ dysfunction syndrome. An acute systemic inflammatory response seems to play an integral role in the development of such complications providing the potential for massive secondary injury. We show that a contusion injury to the rat brain causes large migration of inflammatory cells (especially macrophages and neutrophils) in the major airways and alveolar spaces at 24 h post-injury, which is associated with enhanced pulmonary leukotriene B4 (LTB4) production within the lung. However, by 2 weeks after injury, a temporal switch occurs and the resolution of inflammation is underway. We provide evidence that 5-lipoxygenase and Cytochrome P450 4Fs (CYP4Fs), the respective enzymes responsible for LTB4 synthesis and breakdown, play crucial roles in setting the cellular concentration of LTB4. Activation of LTB4 breakdown via induction of CYP4Fs, predominantly in the lung tissue, serves as an endogenous signal to ameliorate further secondary damage. In addition, we show that CYP4Fs are localized primarily in the airways and pulmonary endothelium. Given the fact that adherence to the microvascular endothelium is an initial step in neutrophil diapedesis, the temporally regulated LTB4 clearance in the endothelium presents a novel focus for treatment of pulmonary inflammation after injury.
机译：已知颅脑外伤会引起多种继发作用，从而导致多器官功能障碍综合征。急性全身性炎症反应似乎在此类并发症的发展中起着不可或缺的作用，提供了大规模继发性损伤的可能性。我们显示，对大鼠脑的挫伤性损伤在损伤后24小时内在主要气道和肺泡腔内引起炎性细胞（尤其是巨噬细胞和嗜中性白细胞）的大量迁移，这与肺内白三烯B4（LTB4）产生增强有关。肺。然而，在受伤后2周，发生了暂时的切换，炎症的消退正在进行中。我们提供证据表明5-脂氧合酶和细胞色素P450 4Fs（CYP4Fs）是负责LTB4合成和分解的各自酶，在设定LTB4的细胞浓度中起关键作用。通过主要在肺组织中诱导CYP4Fs来激活LTB4分解，是一种内源性信号，可减轻进一步的继发性损伤。此外，我们表明CYP4Fs主要位于气道和肺内皮。鉴于对微血管内皮的粘附是嗜中性白血球渗出的第一步，因此内皮中时间调节的LTB4清除率成为治疗损伤后肺部炎症的新焦点。

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