Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated inflammatory response to pathogens. Bioinformatics and transcriptomics studies contribute to get a better understanding of the pathogenesis of sepsis. These studies revealed differentially expressed genes (DEGs) in sepsis involved in several pathways. Here we investigated the gene expression profiles of blood leukocytes using three microarray datasets of sepsis secondary to pneumonia, focusing on the heme/hemoglobin metabolism pathway. We demonstrate that the heme/hemoglobin metabolism pathway was found to be enriched in these three cohorts with four common genes (ALAS2, AHSP, HBD, and CA1). Several studies show that these four genes are involved in the cytoprotection of non-erythrocyte cells in response to different stress conditions. The upregulation of heme/hemoglobin metabolism in sepsis might be a protective response of white cells to the hostile environment present in septic patients (follow-up samples).

中文翻译：

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肺炎继发脓毒症中与血红素-血红蛋白代谢途径相关的遗传特征。

脓毒症被定义为由对病原体的炎症反应失调引起的危及生命的器官功能障碍。生物信息学和转录组学研究有助于更好地了解脓毒症的发病机制。这些研究揭示了脓毒症中的差异表达基因（DEG）涉及多种途径。在这里，我们使用肺炎继发脓毒症的三个微阵列数据集研究了血液白细胞的基因表达谱，重点关注血红素/血红蛋白代谢途径。我们证明，血红素/血红蛋白代谢途径在这三个具有四个常见基因（ALAS2、AHSP、HBD 和 CA1）的队列中富集。多项研究表明，这四种基因参与非红细胞细胞响应不同应激条件的细胞保护。脓毒症中血红素/血红蛋白代谢的上调可能是白细胞对脓毒症患者中存在的敌对环境的保护性反应（后续样本）。