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门静脉内脂多糖会抑制肺部抗菌防御机制。

Intraportal lipopolysaccharide suppresses pulmonary antibacterial defense mechanisms.

作者信息

Mason C M, Dobard E, Summer W R, Nelson S

机构信息

Pulmonary/Critical Care Medicine, Louisiana State University School of Medicine, New Orleans, USA.

出版信息

J Infect Dis. 1997 Nov;176(5):1293-302. doi: 10.1086/514125.

DOI:10.1086/514125
PMID:9359731
Abstract

Translocation of enteric bacteria or their components (or both) has been postulated to play a role in precipitating sepsis or the systemic inflammatory response syndrome. To simulate the effects of translocation on pulmonary host defenses, lipopolysaccharide was injected into the portal vein of normal rats that were subsequently challenged by aerosol inoculation with Pseudomonas aeruginosa. Injection of LPS into the portal vein resulted in increased serum tumor necrosis factor (TNF)-alpha levels and reduction in lung clearance of P. aeruginosa after aerosol challenge. There were corresponding reductions in alveolar neutrophil recruitment, diminished alveolar macrophage phagocytosis and superoxide anion (O2-) production, and diminished lung TNF recovered by bronchoalveolar lavage. Furthermore, prior intravenous injection of recombinant TNF-alpha reproduced the defective bacterial clearance, the altered recruitment of airspace neutrophils, and the defective alveolar macrophage phagocytosis. Thus, systemic TNF-alpha is important in altering pulmonary defenses, and this work supports the concept that bacterial translocation may adversely affect host defenses in distant organs.

摘要

肠道细菌或其成分(或两者)的移位被认为在引发败血症或全身炎症反应综合征中起作用。为了模拟移位对肺部宿主防御的影响,将脂多糖注入正常大鼠的门静脉,随后用铜绿假单胞菌进行气溶胶接种攻击。向门静脉注射脂多糖导致血清肿瘤坏死因子(TNF)-α水平升高,且在气溶胶攻击后铜绿假单胞菌的肺清除率降低。相应地,肺泡中性粒细胞募集减少,肺泡巨噬细胞吞噬作用和超氧阴离子(O2-)产生减少,通过支气管肺泡灌洗回收的肺TNF减少。此外,预先静脉注射重组TNF-α可再现细菌清除缺陷、气腔中性粒细胞募集改变以及肺泡巨噬细胞吞噬作用缺陷。因此,全身性TNF-α在改变肺部防御方面很重要,这项研究支持细菌移位可能对远处器官的宿主防御产生不利影响这一概念。

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