Gharib Sina A, Mar Daniel, Bomsztyk Karol, Denisenko Oleg, Dhanireddy Shireesha, Liles W Conrad, Altemeier William A
*Computational Medicine Core †Center for Lung Biology ‡Division of Pulmonary and Critical Care Medicine §Department of Medicine, University of Washington, Seattle, Washington.
Shock. 2016 Feb;45(2):148-56. doi: 10.1097/SHK.0000000000000507.
Sepsis-induced multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in critically ill patients and remains impervious to most therapeutic interventions. We utilized a clinically relevant murine model of systemic inflammatory response syndrome (SIRS) during early MODS induced by ventilator-associated pneumonia to systematically delineate pathways dysregulated in lung, liver, and kidney. We focused on processes commonly activated across at-risk organs and constructed an SIRS-associated network based on connectivity among the gene members of these functionally coherent pathways. Our analyses led to the identification of several putative drivers of early MODS whose expression was regulated by epidermal growth factor receptor. Our unbiased, integrative method is a promising approach to unravel mechanisms in system-wide disorders afflicting multiple compartments such as sepsis-induced MODS, and identify putative therapeutic targets.
脓毒症诱导的多器官功能障碍综合征(MODS)是危重症患者发病和死亡的主要原因,并且对大多数治疗干预仍无反应。我们利用呼吸机相关性肺炎诱导的早期MODS期间具有临床相关性的全身性炎症反应综合征(SIRS)小鼠模型,系统地描绘肺、肝和肾中失调的通路。我们专注于在高危器官中共同激活的过程,并基于这些功能相关通路的基因成员之间的连通性构建了一个SIRS相关网络。我们的分析导致鉴定出几种早期MODS的假定驱动因子,其表达受表皮生长因子受体调节。我们的无偏整合方法是一种很有前景的方法,可用于揭示诸如脓毒症诱导的MODS等影响多个器官系统的全系统疾病的机制,并确定假定的治疗靶点。