Acute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thought to result from noradrenergic overactivation and excess glucocorticoid release via hypothalamus-pituitary-adrenal axis stimulation. Instead of consecutive hypothalamus-pituitary-adrenal axis activation, we report that acute SCI in mice induced suppression of serum norepinephrine and concomitant increase in cortisol, despite suppressed adrenocorticotropic hormone, indicating primary (adrenal) hypercortisolism. This neurogenic effect was more pronounced after high-thoracic level (Th1) SCI disconnecting adrenal gland innervation, compared with low-thoracic level (Th9) SCI. Prophylactic adrenalectomy completely prevented SCI-induced glucocorticoid excess and lymphocyte depletion but did not prevent pneumonia. When adrenalectomized mice were transplanted with denervated adrenal glands to restore physiologic glucocorticoid levels, the animals were completely protected from pneumonia. These findings identify a maladaptive sympathetic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic normalization of the glucocorticoid and catecholamine imbalance in SCI patients could be a strategy to prevent detrimental infections.

中文翻译：

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脊髓损伤诱导的免疫缺陷是由交感神经内分泌肾上腺反射介导的。

急性脊髓损伤（SCI）导致全身免疫抑制和威胁生命的感染，被认为是由于去甲肾上腺素过度激活和通过下丘脑-垂体-肾上腺轴刺激释放过量的糖皮质激素所致。代替连续的下丘脑-垂体-肾上腺轴激活，我们报道了小鼠急性SCI诱导了血清去甲肾上腺素的抑制和皮质醇的增加，尽管肾上腺皮质激素被抑制，表明原发性（肾上腺）皮质醇过多。与低胸水平（Th9）SCI相比，高胸水平（Th1）SCI断开肾上腺神经支配后，这种神经源性作用更加明显。预防性肾上腺切除术可以完全预防SCI诱导的糖皮质激素过多和淋巴细胞耗竭，但不能预防肺炎。当将肾上腺切除的小鼠移植去神经支配的肾上腺以恢复生理性糖皮质激素水平时，就完全保护了动物免受肺炎的侵害。这些发现确定了SCI后适应不良的交感神经内分泌肾上腺反射介导的免疫抑制，这暗示SCI患者中糖皮质激素和儿茶酚胺失衡的治疗正常化可能是预防有害感染的策略。