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Lung Microbiota Predict Clinical Outcomes in Critically Ill Patients.

肺部菌群预测危重患者的临床结局。

  • 影响因子:5.24
  • DOI:10.1164/rccm.201907-1487OC
  • 作者列表:"Dickson RP","Schultz MJ","van der Poll T","Schouten LR","Falkowski NR","Luth JE","Sjoding MW","Brown CA","Chanderraj R","Huffnagle GB","Bos LDJ","BASIC Consortium.
  • 发表时间:2020-01-24
Abstract

RATIONALE:Recent studies have revealed that in critically ill patients, lung microbiota are altered and correlate with alveolar inflammation. The clinical significance of altered lung bacteria in critical illness is unknown. OBJECTIVES:To determine if clinical outcomes of critically ill patients are predicted by features of the lung microbiome at the time of admission. METHODS:We performed a prospective observational cohort study in an intensive care unit (ICU) at a university hospital. Lung microbiota were quantified and characterized using droplet digital PCR and bacterial 16S rRNA gene sequencing. Primary predictors were the bacterial burden, community diversity, and community composition of lung microbiota. The primary outcome was ventilator-free days, determined at 28 days post admission. MEASUREMENTS AND MAIN RESULTS:Lungs of 91 critically ill patients were sampled using miniature-bronchoalveolar lavage within 24 hours of ICU admission. Patients with increased bacterial lung bacterial burden had fewer ventilator-free days (HR 0.43, CI 0.21-0.88), which remained significant when controlled for pneumonia and severity of illness. The community composition of lung bacteria predicted ventilator-free days (P=0.003), driven by the presence of gut-associated bacteria (e.g. Lachnospiraceae and Enterobacteriaceae spp.). Detection of gut-associated bacteria was also associated with the presence of the acute respiratory distress syndrome. CONCLUSIONS:Key features of the lung microbiome (bacterial burden, enrichment with gut-associated bacteria) predict outcomes in critically ill patients. The lung microbiome is an understudied source of clinical variation in critical illness, and represents a novel therapeutic target for the prevention and treatment of acute respiratory failure.

摘要

原理: 最近的研究表明,在危重患者中,肺部微生物群发生改变,并与肺泡炎症相关。危重病中肺部细菌改变的临床意义尚不清楚。 目的: 确定危重患者的临床结局是否通过入院时肺部微生物组的特征来预测。 方法: 我们在大学医院的重症监护病房 (ICU) 进行了一项前瞻性观察性队列研究。使用液滴数字 PCR 和细菌 16 S rRNA 基因测序对肺部菌群进行定量和表征。主要预测因素是肺部菌群的细菌负担、群落多样性和群落组成。主要结局为无呼吸机天数,在入院后 28 天确定。 测量和主要结果: 在入住 ICU 的 24 小时内,使用微型支气管肺泡灌洗对 91 例危重患者的肺进行采样。肺部细菌负荷增加的患者无呼吸机天数较少 (HR 0.43,CI 0.21-0.88),当控制肺炎和疾病严重程度时,无呼吸机天数仍然显著。肺部细菌的群落组成预测无呼吸机天数 (P = 0.003),由肠道相关细菌 (如 lachnosperaceae 和肠杆菌科 spp.) 的存在驱动。肠道相关细菌的检测也与急性呼吸窘迫综合征的存在有关。 结论: 肺部微生物组的关键特征 (细菌负荷,肠道相关细菌富集) 可预测危重患者的预后。肺微生物组是危重病临床变异的研究来源,代表了预防和治疗急性呼吸衰竭的新治疗靶点。

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影响因子:3.89
发表时间:2020-01-31
DOI:10.1002/jcp.29586
作者列表:["Cong Z","Li D","Tao Y","Lv X","Zhu X"]

METHODS::Acute respiratory distress syndrome (ARDS), characterized by acute hypoxic respiratory dysfunction or failure, is a manifestation of multiple organ failure in the lung, and the most common risk factor is sepsis. We previously showed that blocking α2 -adrenoceptor (α2 -AR) could attenuate lung injury induced by endotoxin in rats. α2A -adrenoceptor (α2A -AR), a subtype of α2 -AR plays a key role in inflammatory diseases, but the mechanism remains unknown. Here, we explored the effect of BRL-44408 maleate (BRL), a specific α2A -AR antagonist, on cecal ligation puncture (CLP)-induced ARDS in rats and the underlying mechanism. Preadministration of BRL-44408 maleate significantly alleviated CLP-induced histological injury, macrophage infiltration, inflammatory response, and wet/dry ratio in lung tissue. However, there was no statistical difference in survival rate between the CLP and CLP+BRL groups. Extracellular regulated protein kinase (ERK1/2), p38MAPK, and p65 were activated in the CLP group, and BRL-44408 maleate inhibited the activation of these signal molecules, c-Jun N-terminal kinase (JNK) and protein kinase A (PKA) showed no changes in activation between these two groups. BRL-44408 maleate decreased lipopolysaccharide (LPS)-induced expression of cytokines in NR8383 rat alveolar macrophages and reduced phosphorylation of ERK1/2, p38MAPK, and p65. JNK and PKA were not influenced by LPS. Together, these findings suggest that antagonism of α2A -AR improves CLP-induced acute lung injury and involves the downregulation of ERK1/2, p38MAPK, and p65 pathway independent of the activation of JNK and PKA.

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