Kawasaki Disease Patient Stratification and Pathway Analysis Based on Host Transcriptomic and Proteomic Profiles.
Kawasaki Disease Patient Stratification and Pathway Analysis Based on Host Transcriptomic and Proteomic Profiles.
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川崎疾病患者分层和途径分析基于宿主转录组和蛋白质组学特征。
DOI：
10.3390/ijms22115655
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发表时间：
2021-05-26
影响因子：
5.6
通讯作者：
On Behalf Of The Perform Consortium
中科院分区：
文献类型：
--
作者：
Jackson H;Menikou S;Hamilton S;McArdle A;Shimizu C;Galassini R;Huang H;Kim J;Tremoulet A;Thorne A;Fischer R;de Jonge MI;Kuijpers T;Wright V;Burns JC;Casals-Pascual C;Herberg J;Levin M;Kaforou M;On Behalf Of The Perform Consortium
川崎（KD）是一种儿童期急性炎症性疾病，尽管已经提出了各种KD的触发因素，但其病因仍不清楚。宿主组学谱提供了对宿主对感染和炎症的反应的深入了解，同时询问多个组学水平提供了更全面的画面。我们使用差异丰度分析、途径分析、聚类和分类技术，通过比较KD儿童与细菌和病毒感染儿童的组学谱，在转录组和蛋白质组水平上探索KD中的宿主反应是否与细菌或病毒感染的反应更相似。KD患者激活的途径包括参与抗病毒和抗细菌反应的途径。无监督聚类显示，大多数KD患者在两个组学水平上与细菌患者聚类，而对细菌和病毒感染特异性的诊断特征的应用揭示，许多转录组KD样品具有细菌或病毒感染的低概率，这表明KD可能由不典型于常见细菌或病毒感染的不同过程触发。基于KD期间的转录组学和蛋白质组学反应的聚类揭示了KD患者在两个组学水平上的三个聚类，表明KD期间的炎症反应内的异质性。观察到的异质性可能反映了宿主对共同触发因素的反应差异，或取决于条件的不同触发因素的变化。
The aetiology of Kawasaki disease (KD), an acute inflammatory disorder of childhood, remains unknown despite various triggers of KD having been proposed. Host ‘omic profiles offer insights into the host response to infection and inflammation, with the interrogation of multiple ‘omic levels in parallel providing a more comprehensive picture. We used differential abundance analysis, pathway analysis, clustering, and classification techniques to explore whether the host response in KD is more similar to the response to bacterial or viral infections at the transcriptomic and proteomic levels through comparison of ‘omic profiles from children with KD to those with bacterial and viral infections. Pathways activated in patients with KD included those involved in anti-viral and anti-bacterial responses. Unsupervised clustering showed that the majority of KD patients clustered with bacterial patients on both ‘omic levels, whilst application of diagnostic signatures specific for bacterial and viral infections revealed that many transcriptomic KD samples had low probabilities of having bacterial or viral infections, suggesting that KD may be triggered by a different process not typical of either common bacterial or viral infections. Clustering based on the transcriptomic and proteomic responses during KD revealed three clusters of KD patients on both ‘omic levels, suggesting heterogeneity within the inflammatory response during KD. The observed heterogeneity may reflect differences in the host response to a common trigger, or variation dependent on different triggers of the condition.
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影响因子：
3.7
作者：
Gold L;Ayers D;Bertino J;Bock C;Bock A;Brody EN;Carter J;Dalby AB;Eaton BE;Fitzwater T;Flather D;Forbes A;Foreman T;Fowler C;Gawande B;Goss M;Gunn M;Gupta S;Halladay D;Heil J;Heilig J;Hicke B;Husar G;Janjic N;Jarvis T;Jennings S;Katilius E;Keeney TR;Kim N;Koch TH;Kraemer S;Kroiss L;Le N;Levine D;Lindsey W;Lollo B;Mayfield W;Mehan M;Mehler R;Nelson SK;Nelson M;Nieuwlandt D;Nikrad M;Ochsner U;Ostroff RM;Otis M;Parker T;Pietrasiewicz S;Resnicow DI;Rohloff J;Sanders G;Sattin S;Schneider D;Singer B;Stanton M;Sterkel A;Stewart A;Stratford S;Vaught JD;Vrkljan M;Walker JJ;Watrobka M;Waugh S;Weiss A;Wilcox SK;Wolfson A;Wolk SK;Zhang C;Zichi D
通讯作者：
Zichi D
影响因子：
5.2
作者：
CURTIS, N;ZHENG, R;LEVIN, M
通讯作者：
LEVIN, M
影响因子：
36.4
作者：
Davies, Patrick;Evans, Claire;Ramnarayan, Padmanabhan
通讯作者：
Ramnarayan, Padmanabhan
影响因子：
22.4
作者：
HUBERT, LJ;LEVIN, JR
通讯作者：
LEVIN, JR
影响因子：
36.4
作者：
Goetzinger, Florian;Santiago-Garcia, Begona;Tebruegge, Marc
通讯作者：
Tebruegge, Marc