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雾化吸入抗生素在支气管扩张症中的应用

支气管扩张症(简称支扩)是一种慢性肺部疾病，特征性地表现为支气管异常、持久的扩张和破坏，临床处理困难。虽然支扩的病因多种多样，但细菌性感染和持续性炎症是其典型病变，且反复发生，导致病情不断恶化。临床表现主要为发热、咯脓性痰，并常伴有胸痛和咯血。在支扩患者的痰中最常分离培养出的细菌是流感嗜血杆菌、肺炎链球菌、金黄色葡萄球菌和铜绿假单胞菌，其中铜绿假单胞菌是病程晚期最常见也是最难处理的感染病原体，往往难以清除，并与病情的加重和恶化密切相关，与其他病原体感染相比可导致更快的肺功能和生活质量的下降[1]。

Acinetobacter Pulmonary Infection：How to Handle It Correctly？

自上世纪90 年代以来, 多耐药非发酵革兰阴性杆菌开始成为医院感染的重要病原菌, 并迅速增加, 其中不动杆菌( Acinetobacter) 尤其令人关注。鲍曼不动杆菌( Acinetobacter baumannii) 或称鲍曼-醋酸钙不动杆菌复合群, 占不动杆菌的80% ～90% , 是不动杆菌中引起人类感染的主要菌群, 具有极强的环境适应能力、获得外源性耐药基因的能力及播散性, 因而被称为21 世纪革兰阴性菌中的“耐甲氧西林金黄色葡萄球菌( MRSA) ”, 值得引起临床医生的重视。

De-escalation therapy in severe pulmonary infectious diseases

抗生素的降阶梯治疗（de-escalation therapy）是近年来提出的用于治疗重症肺部感染的一个策略，在临床研究和实践中能够有效地提高重症感染治疗的成功率，降低病死率，同时降低住院时间和费用，是感染治疗策略的一大进展。本文就这一策略的概念演变和应用时机作一介绍

丙酮酸乙酯对脓毒症保护作用研究进展

丙酮酸是糖酵解的终产物及三羧酸循环的起始物，是机体能量代谢的主要中间产物，当机体氧供应充足时丙酮酸在线粒体内氧化为乙酰辅酶A，维持三羧酸循环；当氧供应不足时在乳酸脱氢酶作用下直接转化成乳酸，迅速为机体供能。丙酮酸在细胞内可能作为内源性抗氧化物，无需酶就能降解过氧化氢，产生二氧化碳和水。丙酮酸消除过氧化氢的反应高效迅速。除了清除过氧化氢，丙酮酸也能清除羟基、一氧化氮等其他活性氧。丙酮酸乙酯（EP）是丙酮酸亲脂性的酯化物，在抗炎、抗凝及安全性方面明显优于丙酮酸[1]

Mechanisms of Aspergillus Fumigatus Invasion

随着免疫抑制人群的增多、检测技术的发展, 深部真菌感染日益受到人们的关注。真菌中的曲霉属成了这些免疫功能低下患者致病性感染的重要原因, 而烟曲霉在侵袭性曲霉病例中最常见。侵袭力是烟曲霉菌极为重要的致病原因;病原菌侵入上皮、内皮细胞等组织细胞后才导致了可怕的侵袭性感染。从上世纪90 年代来, 对于侵袭的研究已逐步深入, 为探讨复杂的致病机制打下了基础。侵袭性烟曲霉病一般的致病过程认为是烟曲霉孢子被宿主吸入下呼吸道, 侵入呼吸道上皮细胞后发育成菌丝, 菌丝进一步生长, 可侵入血管、进入血液, 造成全身播散[ 1] 。因此曲霉与宿主细胞( 上皮细胞、内皮细胞等) 的相互作用成了致病过程的重要环节。目前对病原体与宿主细胞作用的研究取得了一些进展, 对阐明致病机制、研究治疗靶点等有重要意义。

气道防御屏障

人类气道从功能上可以分为四个解剖节段: 上呼吸道( 鼻咽部, Ⅰ段) 、导气段( 从咽到终末支气管, Ⅱ 段) 、呼吸性支气管( Ⅲ段) 、肺泡管和肺泡( Ⅳ段) 。随着管径变细, 气道上皮逐渐由假复层上皮变为单层上皮, 上皮细胞的高度也逐渐变低, 杯状细胞数量逐渐变少直至消失。其结构不同, 决定了功能的不同。肺泡是进行气体交换的场所, 表面只覆有单层肺泡上皮细胞, 容易受到外界微生物或吸入颗粒的损伤, 因此Ⅰ、Ⅱ和Ⅲ段气道的主要功能是净化吸入气体, 降低肺泡接触损伤因素的可能性, 从而维持肺泡正常气体交换功能。Ⅰ段可清除直径gt; 10 μm的颗粒,Ⅱ、Ⅲ段可清除直径gt;0. 5 μm的颗粒, 直径lt; 0. 5 μm的颗粒可进入肺泡。为保障在清除过程中空气中抗原物质不至于引起气道损伤或感染,气道黏膜存在着屏障功能。我们提出用“气道防御屏障”来概括各种屏障因素。该屏障不仅包括以前所认为的由黏液冲刷、纤毛运动以及气道上皮的紧密连接组成的简单的机械屏障, 而且包括由多种免疫细胞和气道上皮细胞参与的免疫屏障。

The Interpretation of Diagnosis and Treatment Guidelines of Hospital Acquired Pneumonia/Ventilator-associated Pneumonia Guideline

支气管扩张的诊断和治疗进展

Diagnosis and treatment of pulmonary infection with rare pathogen

In recent years, with the wide application of metagenomics next-generation sequencing, more and more rare pathogens have been detected in our clinical work, including non-tuberculous Mycobacterium, Corynebacterium, Fusarium, Cryptococcus pneumoniae, human herpes virus, torque teno virus, parvovirus, Tropheryma whipplei, Bartonella, Chlamydia psittaci, etc. It is difficult to determine whether these rare pathogens are clinically significant and need treatment. This article puts forward some suggestions and discussions on the diagnosis and treatment of pulmonary infections with some rare pathogens.

Gene Expression of TLR2 in Lung and Its Potential Signal Transduction Mechanism in a Mouse Model of Chlamydia Pneumoniae Pneumonitis

Objective To investigate changes of TLR2 mRNA expression in lung of a mouse model of Chlamydia Pneumoniae pneumonitis, and to explore the possible mechanism of signal transduction. Methods Ninety-six male C3H/HeJ mice were randomly divided into four groups as follows: a control group, a model group, a SB203580 intervened group, and a pyrrolidine dithiocarbamate( PDTC) intervened group. Chlamydia Pneumoniae pneumonitis was induced by intranasally inoculated with 4. 0 ×106 IFU/mL of C. Pneumoniae per mouse in the model group and two intervened groups. Then the intervened groups were intraperitoneally injected with the p38MAPK inhibitor SB203580 and nuclear factor kappa B ( NF-κB)inhibitor PDTC, respectively. Six mice in each group were randomly killed in 1st, 4th, 7th and 14th day. The expressional changes of TLR2 mRNA in the mice lung tissue were measured by semi-quantitative RT-PCR. The concentrations of TNF-α in the lung homogenate were measured by ELISA. Results TLR2 mRNA expression in the lung tissue significantly increased after C. Pneumoniae infection, peaking at 4th and 7th days, then decreased after 14th day. Tumor necrosis factor-α( TNF-α) was also elevated in the lung tissue after C. Pneumoniae challenging. Both SB203580 and PDTC treatment effectively inhibited TNF-αand TLR2 mRNA expressions in lung. The inhibitory effect was more obvious by SB203580 treatment. Conclusion C. Pneumoniae can upregulate the expressions of TLR2 and TNF-α in lung, and TLR2/MAPK and TLR2 /NF-κB signal pathways may be involved in Chlamydia Pneumoniae pneumonitis.