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炎症与肺炎:为何有些人更易患病?

Inflammation and Pneumonia: Why Are Some More Susceptible than Others?

机构信息

Pulmonary Center, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02115, USA.

出版信息

Clin Chest Med. 2018 Dec;39(4):669-676. doi: 10.1016/j.ccm.2018.07.002.

DOI:10.1016/j.ccm.2018.07.002
PMID:30390740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6221464/
Abstract

Pneumonia is an important cause of morbidity and mortality. However, pneumonia is an unusual outcome of respiratory infection. Most of the time, microbes in the lung can be controlled by a combination of constitutive and recruited defense mechanisms. Inflammation is a key component of recruited defenses. Variations in inflammation that influence pneumonia susceptibility and severity are considered here.

摘要

肺炎是发病率和死亡率的重要原因。然而,肺炎是呼吸道感染的一种不常见的结果。大多数时候,肺部的微生物可以通过组成性和募集的防御机制的组合来控制。炎症是募集防御的关键组成部分。在这里考虑影响肺炎易感性和严重程度的炎症变化。

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本文引用的文献

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Integrative Physiology of Pneumonia.肺炎的整体生理学
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Regionally compartmentalized resident memory T cells mediate naturally acquired protection against pneumococcal pneumonia.区域性隔室化的固有记忆 T 细胞介导对肺炎球菌性肺炎的天然获得性保护。
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Age-Associated Microbial Dysbiosis Promotes Intestinal Permeability, Systemic Inflammation, and Macrophage Dysfunction.年龄相关的微生物失调促进肠道通透性、全身炎症和巨噬细胞功能障碍。
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Deletion of Irf3 and Irf7 Genes in Mice Results in Altered Interferon Pathway Activation and Granulocyte-Dominated Inflammatory Responses to Influenza A Infection.小鼠中Irf3和Irf7基因的缺失导致甲型流感病毒感染时干扰素通路激活改变以及以粒细胞为主的炎症反应。
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