The respiratory tract microbiome and lung inflammation: a two-way street.
The respiratory tract microbiome and lung inflammation: a two-way street.
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DOI：
10.1038/mi.2016.108
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发表时间：
2017-03
影响因子：
8
通讯作者：
Lukacs NW
中科院分区：
文献类型：
--
作者：
Huffnagle GB;Dickson RP;Lukacs NW
肺不是无菌的，也不是没有细菌的;相反，它们有一个独特的微生物组，其组成由与胃肠道不同的生态规则驱动。在疾病期间，群落组成经常向γ-变形菌门转变，γ-变形菌门是包含许多常见的肺相关革兰氏阴性“病原体”的细菌类别。宿主炎症的许多副产物是这些细菌的生长因子。由于粘液和血管通透性的存在，肺中细菌的细胞外营养供应在健康期间受到严重限制，显著增加。虽然γ-变形菌从气道炎症中获益，但它们也编码促进炎症的分子组分，可能产生周期性炎症机制。相比之下，普雷沃菌属的物种，常规收购通过微抽吸从口腔可能参与气道的免疫稳态。未来的研究领域包括确定特定肺部疾病（1）改变的肺部微生物组是否引发疾病发病机制，促进慢性炎症，或者仅仅是损伤和炎症的标志物，（2）是否可以治疗性地操纵肺部微生物组以改变疾病进展，（3）哪些分子炎症反应期间产生的代谢物促进跨界信号传导，以及（4）肺炎期间肺“生态系统”如何崩溃，由单一病原体主导。
The lungs are not sterile or free from bacteria; rather, they harbor a distinct microbiome whose composition is driven by different ecological rules than for the gastrointestinal tract. During disease, there is often a shift in community composition towards Gammaproteobacteria, the bacterial class that contains many common lung-associated gram-negative “pathogens.” Numerous byproducts of host inflammation are growth factors for these bacteria. The extracellular nutrient supply for bacteria in the lungs, which is severely limited during health, markedly increases due to the presence of mucus and vascular permeability. While Gammaproteobacteria benefit from airway inflammation, they also encode molecular components that promote inflammation, potentially creating a cyclical inflammatory mechanism. In contrast, Prevotella species that are routinely acquired via microaspiration from the oral cavity may participate in immunologic homeostasis of the airways. v Areas of future research include determining for specific lung diseases (1) whether an altered lung microbiome initiates disease pathogenesis, promotes chronic inflammation, or is merely a marker of injury and inflammation, (2) whether the lung microbiome can be manipulated therapeutically to change disease progression, (3) what molecules (metabolites) generated during an inflammatory response promote cross-kingdom signaling, and (4) how the lung “ecosystem” collapses during pneumonia, to be dominated by a single pathogen.
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影响因子：
8.3
作者：
Dickson, Robert P.;Erb-Downward, John R.;Curtis, Jeffrey L.
通讯作者：
Curtis, Jeffrey L.
DOI：
10.1126/science.1198469
发表时间：
2011-01-21
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Atarashi K;Tanoue T;Shima T;Imaoka A;Kuwahara T;Momose Y;Cheng G;Yamasaki S;Saito T;Ohba Y;Taniguchi T;Takeda K;Hori S;Ivanov II;Umesaki Y;Itoh K;Honda K
通讯作者：
Honda K
DOI：
10.1073/pnas.1310750111
发表时间：
2014-01-14
影响因子：
11.1
作者：
Fujimura, Kei E.;Demoor, Tine;Lynch, Susan V.
通讯作者：
Lynch, Susan V.
影响因子：
18.2
作者：
Dickson RP;Erb-Downward JR;Martinez FJ;Huffnagle GB
通讯作者：
Huffnagle GB
DOI：
10.1016/j.jaci.2010.10.048
发表时间：
2011-02
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Huang YJ;Nelson CE;Brodie EL;Desantis TZ;Baek MS;Liu J;Woyke T;Allgaier M;Bristow J;Wiener-Kronish JP;Sutherland ER;King TS;Icitovic N;Martin RJ;Calhoun WJ;Castro M;Denlinger LC;Dimango E;Kraft M;Peters SP;Wasserman SI;Wechsler ME;Boushey HA;Lynch SV;National Heart, Lung, and Blood Institute's Asthma Clinical Research Network
通讯作者：
National Heart, Lung, and Blood Institute's Asthma Clinical Research Network