For a study, researchers sought to find differences between asymptomatic controls and those with chronic orchialgia (CO) in the expression of neuroinflammatory genes.
At the time of microscopic spermatic cord denervation, the vas deferens, spermatic cord fascia, blood, and urine of nine men with CO and seven asymptomatic controls were obtained. With the use of the NanoString Human Neuroinflammation panel, RNA was extracted and examined. Data were standardized, and fold differences in gene expression and enriched pathways compared to asymptomatic controls were found. If there was a change in gene expression of less than 2-fold and the P-value <.05. compared to controls, it was deemed significant.
The median symptom duration was 12 months, and the average patient age was 51 years. In the vas deferens, 26 genes had substantially varied expression levels. The most significant variation was found in cFos, a nociceptive pain marker (30.2-fold change, P<.000001). Nerve activity, matrix remodeling, and innate immune responses were among the enriched pathways in the vas deferens. S100A12 (11-fold, inducer of innate immune response) and cFos were the genes with the largest differential expression in the fascia (38-fold, P=.000002). Nerve activity and inflammation were present in the fascia’s enhanced pathways. There were 95 genes that were differently expressed in urine, but none were significantly expressed in blood.
Different neuroinflammatory genes express themselves differently in tissue and urine in men with CO compared to healthy controls. The findings showed molecular alterations in neuropathic pain that might lead to the discovery of biomarkers and the development of novel treatments, and they validate pathologic changes in a tissue targeted by denervation surgery.