Department of Pain & Translational Symptom Science and Center to Advance Chronic Pain Research, University of Maryland School of Nursing, Baltimore, Maryland, United States of America.
University of Delaware School of Nursing, Newark, Delaware, United States of America.
PLoS One. 2019 May 16;14(5):e0216539. doi: 10.1371/journal.pone.0216539. eCollection 2019.
The mechanisms underlying the transition from acute to chronic pain remain unclear. Here, we sought to characterize the transcriptome associated with chronic low back pain as well as the transcriptome of the transition from acute to chronic low back pain. For the analysis, we compared the whole blood transcriptome of: (a) patients at the onset of low back pain who no longer had pain within 6 weeks after onset (acute) with patients who developed chronic low back pain at 6 months (chronic T5); and, (b) patients at the onset of low back pain (chronic T1) who developed chronic pain at 6 months with healthy pain-free (normal) controls. The majority of differentially expressed genes were protein coding. We illustrate a unique chronic low back pain transcriptome characterized by significant enrichment for known pain genes, extracellular matrix genes, and genes from the extended major histocompatibility complex (MHC) genomic locus. The transcriptome of the transition from acute to chronic low back pain was characterized by significant upregulation of antigen presentation pathway (MHC class I and II) genes and downregulation of mitochondrial genes associated with oxidative phosphorylation, suggesting a unique genomic signature of vulnerability to low back pain chronicity.
慢性疼痛形成的机制仍不清楚。在这里,我们试图描述与慢性下腰痛相关的转录组以及从急性到慢性下腰痛转变的转录组。为此分析,我们比较了以下患者的全血转录组:(a)下腰痛发作后 6 周内不再疼痛的患者(急性)与 6 个月后发展为慢性下腰痛的患者(慢性 T5);和(b)下腰痛发作时(慢性 T1)的患者,6 个月后发展为慢性疼痛的患者与健康无痛(正常)对照。差异表达基因大多数是编码蛋白的基因。我们展示了一个独特的慢性下腰痛转录组,其特征是已知疼痛基因、细胞外基质基因和扩展主要组织相容性复合体(MHC)基因组座中的基因显著富集。从急性到慢性下腰痛的转变的转录组特征是抗原呈递途径(MHC 类 I 和 II)基因的显著上调和与氧化磷酸化相关的线粒体基因的下调,这表明对下腰痛慢性易感性的独特基因组特征。