TBI induces splenic B and T cell expansion that contributes to neuroinflammation and neurodegeneration. The vagus nerve, the longest of the cranial nerves, is the predominant parasympathetic pathway allowing the central nervous system (CNS) control over peripheral organs, including regulation of inflammatory responses. One way this is accomplished is by vagus innervation of the celiac ganglion, from which the splenic nerve innervates the spleen. This splenic innervation enables modulation of the splenic immune response, including splenocyte selection, activation, and downstream signaling. Considering that the left and right vagus nerves have distinct courses, it is possible that they differentially influence the splenic immune response following a CNS injury. To test this possibility, immune cell subsets were profiled and quantified following either a left or a right unilateral vagotomy. Both unilateral vagotomies caused similar effects with respect to the percentage of B cells and in the decreased percentage of macrophages and T cells following vagotomy. We next tested the hypothesis that a left unilateral vagotomy would modulate the splenic immune response to a traumatic brain injury (TBI). Mice received a left cervical vagotomy or a sham vagotomy 3 days prior to a fluid percussion injury (FPI), a well-characterized mouse model of TBI that consistently elicits an immune and neuroimmune response. Flow cytometric analysis showed that vagotomy prior to FPI resulted in fewer CLIP+ B cells, and CD4+, CD25+, and CD8+ T cells. Vagotomy followed by FPI also resulted in an altered distribution of CD11bhigh and CD11blow macrophages. Thus, transduction of immune signals from the CNS to the periphery via the vagus nerve can be targeted to modulate the immune response following TBI.

Split cord malformations (SCMs) are rare congenital abnormalities arising from a primary neurulation defect during embryological development of the spinal cord. SCMs can lead to progressively worsening scoliosis and gait difficulties if left untreated. We report on two patients who atypically presented with SCM in adulthood and review previous reports.

The Vagus Nerve is a major component, in conjunction with the spleen, in modulating the systemic anti-inflammatory response. Adrenergic fibers of the splenic nerve innervate the spleen, where they stimulate a distinct population of memory T cells. These memory T cells subsequently release ACh, thereby reducing macrophage activation and inhibiting TNFα. Therefore this pathway, as it relates to the spleen, is a two-neuron circuit: initiating first in the dorsal motor nucleus of the Vagus, subsequently synapsing at the celiac ganglion, and finally synapsing on the memory T cells. There are additional lines of evidence demonstrating cholinergic modulation of immune cells in the spleen. For example emerging evidence supports a regulating role of the vagus nerve in mobilizing marginal zone B cells and their subsequent secretion of antibodies, heralding an innate immune response. However, a direct link between splenic B cell number and the vagus nerve has not been previously established. Therefore, we assessed the effects of a left unilateral vagotomy on total splenocytes and MHCII+/CD11+ B cells in the spleen 3 days after vagotomy. Results The results indicate that at 3 days after left unilateral vagotomy, there is a significant decrease in the overall number of splenocytes. The results also show that this vagotomy results in a trend toward a significant reduction in MHCII+/CD11+ B cells in the spleen. Conclusions Our conclusions based upon these results show that there is a direct influence of left vagus nerve innervation on the number of splenic B cells and that left vagotomy results in an overall decrease in either the proliferation of splenocytes in general including the B-cells, or in cell death of splenocytes including the B cells.