Splenic sympathetic signaling contributes to acute neutrophil infiltration of the injured spinal cord
S Monteiro, AG Pinho, M Macieira… - Journal of …, 2020 - Springer
Journal of Neuroinflammation, 2020•Springer
Background Alterations in the immune system are a complication of spinal cord injury (SCI)
and have been linked to an excessive sympathetic outflow to lymphoid organs. Still
unknown is whether these peripheral immune changes also contribute for the deleterious
inflammatory response mounted at the injured spinal cord. Methods We analyzed different
molecular outputs of the splenic sympathetic signaling for the first 24 h after a thoracic
compression SCI. We also analyzed the effect of ablating the splenic sympathetic signaling …
and have been linked to an excessive sympathetic outflow to lymphoid organs. Still
unknown is whether these peripheral immune changes also contribute for the deleterious
inflammatory response mounted at the injured spinal cord. Methods We analyzed different
molecular outputs of the splenic sympathetic signaling for the first 24 h after a thoracic
compression SCI. We also analyzed the effect of ablating the splenic sympathetic signaling …
Background
Alterations in the immune system are a complication of spinal cord injury (SCI) and have been linked to an excessive sympathetic outflow to lymphoid organs. Still unknown is whether these peripheral immune changes also contribute for the deleterious inflammatory response mounted at the injured spinal cord.
Methods
We analyzed different molecular outputs of the splenic sympathetic signaling for the first 24 h after a thoracic compression SCI. We also analyzed the effect of ablating the splenic sympathetic signaling to the innate immune and inflammatory response at the spleen and spinal cord 24 h after injury.
Results
We found that norepinephrine (NE) levels were already raised at this time-point. Low doses of NE stimulation of splenocytes in vitro mainly affected the neutrophils’ population promoting an increase in both frequency and numbers. Interestingly, the interruption of the sympathetic communication to the spleen, by ablating the splenic nerve, resulted in reduced frequencies and numbers of neutrophils both at the spleen and spinal cord 1 day post-injury.
Conclusion
Collectively, our data demonstrates that the splenic sympathetic signaling is involved in the infiltration of neutrophils after spinal cord injury. Our findings give new mechanistic insights into the dysfunctional regulation of the inflammatory response mounted at the injured spinal cord.
Springer
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