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Abstract Background Spinal cord injury (SCI), which causes loss of sensory and motor function in the body below the level of injury, is a devastating disease of the central nervous system. SCI leads to severe secondary immunosuppression, called SCI-induced immunodeficiency syndrome (SCI-IDS), which is characterized by increased susceptibility to infection and further exacerbates neurological dysfunction. Several studies have suggested that SCI-IDS is an independent risk factor for poor neurological prognosis. SCI-IDS predominantly occurs following injury above the T5 levels and eventually leads to systemic immune failure, possibly via the sympathetic–adrenal medullary axis and the hypothalamic‒pituitary‒adrenal (HPA) axis. However, the mechanism remains unclear. Methods and objectives The concentrations of adrenocorticotropic hormone and cortisol in plasma, as well as changes in sympathetic activity (blood pressure and catecholamine levels in plasma), were assessed in rats in the high-level (T3) spinal cord injury (T3-SCI) group and the low-level (T10) spinal cord injury (T10-SCI) group. Second, the differential regulation of the gene network between the sympathetic–adrenal medullary axis and the HPA axis was explored by histology and multitissue transcriptomics, and the neuroendocrine–immune network associated with SCI-IDS was further elucidated. Results The spleen and thymus gland, which are secondary immune organs, were significantly atrophied in rats in the T3-SCI group, and the white pulp of the spleen was significantly atrophied. The level of cortisol, which is mediated by the adrenal glands, was markedly elevated, but norepinephrine levels were markedly decreased. There was no difference in adrenocorticotropic hormone expression between any of the groups. The transcriptome analysis results showed that the downregulated differentially expressed genes (DEGs) in the T3-SCI group were enriched in the GO term immunoregulation, indicating that splenic immune function was markedly impaired after high-level SCI. The upregulated DEGs in the hypothalamus (hub genes: Nod2, Serpine1, Cebpb, Nfkbil1, Ripk2, Zfp36, Traf6, Akap8, Gfer, Cxcl10, Tnfaip3, Icam1, Fcgr2b, Ager, Dusp10, and Mapkapk2) were significantly enriched in inflammatory pathways, and the downregulated genes (hub genes: Grm4, Nmu, P2ry12, rt1-bb1, Oprm1, Zfhx2, Gpr83, and Chrm2) were enriched in pathways related to inhibitory Gi-mediated G protein-coupled receptor (Gi-GPCR) neurons and neuropeptide changes. The upregulated genes in the adrenal glands (hub genes: Ciart, per2, per3, cry1, and cry2) were enriched in cortisol secretion and circadian rhythm changes, and the downregulated genes (hub genes: IL7r, rt1-bb, rt1-bb1, rt1-da, rt1-ba, cd74, cxcr3, vcam1, ccl5, bin1, and IL8) were significantly enriched in MHC-mediated immune responses. Conclusions To explore the possible mechanism underlying SCI-IDS, this study assessed the differential regulation of the gene network associated with neuroendocrine immunity after SCI. Progressive neuroinflammation spreads after injury, and neurotransmission through Gi-mediated G protein-coupled receptors in the HPA axis and neuropeptide production by the hypothalamus are inhibited. Disruption of the connection between the hypothalamus and the adrenal glands causes autonomous regulation of the adrenal glands, disturbance of circadian rhythm and finally hypercortisolemia, leading to general suppression of peripheral adaptive immunity. Neuraxial nerve inflammation caused by SCI persists indefinitely, blocking nerve repair; persistent system-wide immunosuppression in the periphery results in increased susceptibility to infection, leading to poor neurological prognosis.

Introduction: dysphagia is a common complication of stroke, and serum albumin is widely recognized as a strong prognostic marker of health and/or disease status. However, the correlation between dysphagia and serum albumin levels has not been established. Objectives: to observe the correlation between dysphagia and serum albumin levels and prognosis in patients with stroke. Methods: we performed a retrospective study of patients hospitalized between June 1, 2018, and June 1, 2022. A total of 1,370 patients were enrolled. The patients were divided into two groups: dysphagia and non-dysphagia. Binary logistic regression and multiple linear regression models were used to analyze the correlation between dysphagia, albumin, modified Rankin Scale (mRS), activities of daily living (ADL), and length of hospital stay (LOS). Results: after adjusting for confounding factors, the risk of pneumonia in the dysphagia group was 2.417 times higher than that in the non-dysphagia group (OR = 2.417, 95 % CI: 1.902-3.072, p = 0.000). The risk of mRS ≥ 3 and modified Barthel index (MBI) < 60 in patients with dysphagia was 3.272-fold (OR = 3.272, 95 % CI: 2.508-4.269, p < 0.001) and 1.670-fold (OR = 1.670, 95 % CI: 1.230-2.268, p < 0.001), respectively; and the risk of hypoproteinemia was 2.533 times higher (OR = 2.533, 95 % CI: 1.879-3.414, p = 0.000). Stepwise linear regression showed that dysphagia was significantly correlated with lower albumin levels and higher mRS, lower ADL, and longer LOS in patients with stroke (β = -0.220, β = 0.265, β = -0.210, and β = 0.147, respectively; p < 0.001). Conclusions: dysphagia in patients with stroke is associated with decreased albumin levels and has an impact on its prognosis. [ABSTRACT FROM AUTHOR]