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bronchopneumonia

呼吸

关键词呼吸 疾病 临床疾病

词汇介绍

拓展阅读

解析

bronchopneumonia   英 /,brɒŋkə(ʊ)njuː'məʊnɪə/   美 /,brɑŋkonjʊ'monjə/

       n. [内科] 支气管肺炎

同根词   adj. bronchial 支气管的;bronchitic 支气管炎的;bronchoscopic 支气管镜的

               n. bronchodilator [内科][药] 支气管扩张剂;支气管扩张器

       This abscessing bronchopneumonia has numerous areas of raised, lighter tan appearance which are the areas containing the extensive neutrophilic infiltrates. 脓肿化的支气管肺炎可见大量隆起的浅棕色病灶,病灶中有广泛的中性粒细胞浸润。

概述

支气管肺炎又称小叶肺炎,是一种小儿常见病,尤多见于婴幼儿,也是婴儿时期主要死亡原因之一。肺炎多发生于冬春寒冷季节及气候骤变时,但夏季并不例外。甚至有些华南地区反而在夏天发病较多,患病后免疫力不持久,容易再受感染。支气管肺炎由细菌或病毒引起。 诊断据急性起病、呼吸道症状及体征,一般临床诊断不难。必要时可做X线透视、胸片检查,或咽拭子、气管分泌物细菌培养或病毒分离。其他病原学检查包括抗原和抗体检测。白细胞明显升高和粒细胞增多、血清C反应蛋白升高时有助于细菌性肺炎的诊断。白细胞减低或正常,则多属病

Influenza-mediated reduction of lung epithelial ion channel activity leads to dysregulated pulmonary fluid homeostasis复制标题

流感介导的肺上皮离子通道活性降低导致肺液体稳态失调

发表时间:2018-10-13

影响因子:6.0

作者: Brand Jeffrey D.

期刊:JCI INSIGHT

Severe influenza (IAV) infection can develop into bronchopneumonia and edema, leading to acquired respiratory distress syndrome (ARDS) and pathophysiology. Underlying causes for pulmonary edema and aberrant fluid regulation largely remain unknown, particularly regarding the role of viral-mediated mechanisms.  Multiple lines of evidence indicated ENaC and CFTR dysfunction during the acute infection period; however, only CFTR dysfunction persisted beyond the infection period. ENaC, CFTR, and Na, K-ATPase activities and protein levels were also reduced in virally infected human airway epithelial cells. Reduced ENaC and CFTR led to changes in airway surface liquid morphology of human tracheobronchial cultures and airways of IAV-infected mice. Pharmacologic correction of CFTR function ameliorated IAV-induced physiologic changes. These changes are consistent with mucous stasis and pulmonary edema; furthermore, they indicate that repurposing therapeutic interventions correcting CFTR dysfunction may be efficacious for treatment of IAV lung pathophysiology.

译文

严重流感(IAV)感染可发展成支气管肺炎和水肿,导致获得性呼吸窘迫综合征(ARDS)和病理生理学。肺水肿和异常液体调节的潜在原因在很大程度上仍然是未知的,特别是关于病毒介导机制的作用。多个证据表明急性感染期间ENaC和CFTR功能障碍;然而,只有CFTR功能障碍持续超过感染期。在病毒感染的人呼吸道上皮细胞中ENaC,CFTR和Na,K-ATP酶活性和蛋白质水平也降低。降低的ENaC和CFTR导致IAV感染小鼠的人气管支气管培养物和气道的气道表面液体形态的变化。 CFTR功能的药理学校正改善了IAV诱导的生理变化。这些变化与粘液淤滞和肺水肿一致;此外,他们指出重新利用纠正CFTR功能障碍的治疗干预可能对治疗IAV肺病理生理学有效。