Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Modulation of brain dead induced inflammation by vagus nerve stimulation

ABSTRACT: Because the vagus nerve is implicated in control of inflammation, we investigated if brain death causes impairment of the parasympathetic nervous system, hence contributing to inflammation. Brain death (BD) was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD+STIM) during BD. Intestine, kidney, heart and liver were harvested after 6h. Affymetrix chip- analysis was performed on intestinal RNA. Quantitative PCR was performed on all organs. Serum was collected to assess TNFÎ± concentrations. Renal transplantations were performed to address the influence of vagus nerve stimulation on graft outcome. HRV was significantly lower in BD animals. Vagus nerve stimulation inhibited the increase in serum TNFÎ± concentrations and resulted in down-regulation of a multiplicity of pro-inflammatory genes in intestinal tissue. In renal tissue vagal stimulation significantly decreased the expression of E-selectin, IL1Î² and ITGA6. Renal function was significantly better in recipients that received a graft from a BD+STIM donor. Our study demonstrates impairment of the parasympathetic nervous system during BD and inhibition of serum TNFÎ± through vagal stimulation. Vagus nerve stimulation variably affected gene expression in donor organs and improved renal function in recipients. Gene expression in brain dead (BD) induced rat (with and without vagal stimulation) was compared with that of Non brain-dead ventilated control (NBD)

ORGANISM(S): Rattus norvegicus

SUBMITTER: Benito Yard

PROVIDER: E-GEOD-16483 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Modulation of brain dead induced inflammation by vagus nerve stimulation.

Hoeger S S Bergstraesser C C Selhorst J J Fontana J J Birck R R Waldherr R R Beck G G Sticht C C Seelen M A MA van Son W J WJ Leuvenink H H Ploeg R R Schnuelle P P Yard B A BA

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons 20100105 3

Because the vagus nerve is implicated in control of inflammation, we investigated if brain death (BD) causes impairment of the parasympathetic nervous system, thereby contributing to inflammation. BD was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD + STIM) during BD. Intestine, kidney, heart and liver were recovered after 6 hours. Affymetrix chip-analysis was performed on ...[more]

PMID: 20055812

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Project description:Introduction: The ideal ventilation strategy for patients with massive brain damage requires better elucidation. We hypothesized that in the presence of massive brain injury, a ventilation strategy using low (6 mL/kg) tidal volume (VT) ventilation with open lung positive end-expiratory pressure set according to the minimal static elastance of the respiratory system (LVT/OLPEEP), attenuate the impact of massive brain damage on gas-exchange, respiratory mechanics, lung histology and whole genome alterations compared with high (12 mL/kg) VT and low PEEP ventilation (HVT/LPEEP). Methods: Twenty-eight adult male Wistar rats were randomly assigned to one of four groups: 1) no brain damage (NBD) with LVT/OLPEEP; 2) NBD with HVT/LPEEP; 3) brain damage (BD) with LVT/OLPEEP; and 4) BD with HVT/LPEEP. All animals were mechanically ventilated for six hours. Brain damage was induced by an inflated balloon catheter into the epidural space. Hemodynamics was recorded and blood gas analysis was performed hourly. At the end of the experiment, respiratory system mechanics and lung histology were analysed. Whole genome analysis was performed using Affimetrix gene chips and confirmatory real-time PCR. Results: In NBD, both LVT/OLPEEP and HVT/LPEEP did not affect arterial blood gases, as well as whole genome expression changes and real-time PCR. In BD, LVT/OLPEEP, compared to HVT/LPEEP, reduced lung damage according to histology, genome analysis and real-time PCR with decreased interleukin (IL-6), cytokine-induced neutrophil chemoattractant (CINC)-1 and angiopoietin-4 expressions. LVT/OLPEEP compared to HVT/LPEEP improved overall survival. Conclusions: In BD, LVT/OLPEEP minimizes lung morpho-functional changes and inflammation compared to HVT/LPEEP. LVT/OLPEEP might represent a suitable ventilatory strategy in massive brain damage. 24 Wistar rats - lung samples, 4 groups, 1. non-braindamaged/braindead high tidal volume ventilation, 2. non-braindamaged/braindead best PEEP ventilation, 3. Braindamaged/braindead high tidal volume ventilation, 4. Braindamaged/braindead best PEEP ventilation

Project description:Background: Sepsis can lead to multiple organ damage, and the heart is one of the most vulnerable organs. Vagal nerve stimulation can reduce myocardial injury in sepsis and improve survival rate. However, the relative effect of disparate cell populations on sepsis induced myocardial dysfunction and the low-level tragus stimulation on it, remain unclear. Methods: We used the cardiac single-cell transcriptomic strategy to characterize the cardiac cell population and the network of cells that forms the heart. And we selected all cardiac macrophage from CD45+ cells using single-cell mRNA sequencing data. Then we used echocardiography performing, western blot and immunofluorescence and immunohistochemical technology to verify the data of the single-cell mRNA sequencing results. Results: In single-cell mRNA sequencing data, our analysis provides a comprehensive map of the cardiac cellular landscape uncovering multiple cell populations that contribute to sepsis induced myocardial dysfunction under low-level tragus stimulation. Pseudo timing analysis in single-cell sequencing showed that low level vagal nerve stimulation could induce the transformation of cardiac monocytes into M2 macrophages and play an anti-inflammatory role. After low-level tragus stimulation, the expression of α7nAChR in the heart tissue increased significantly. Echocardiography showed that low-level tragus stimulation could improve the cardiac function of septic myocardial injury of the mice. Comparing with the sepsis group, the expression of interleukin-1β in heart tissue of the mice in sepsis with low-level tragus stimulation group is significantly lower. Conclusion: Low-level tragus stimulation can improve sepsis-induced myocardial dysfunction by promoting cardiac monocytes to M2 macrophages. Goal of the study: In the present study, we aimed to screen macrophages, their crosstalk with other cells, and macrophages associated with cardiac injury and further verify their origins and roles in the septic myocardial injury process and low-level tragus stimulation (LL-TS) to treat septic myocardial dysfunction.

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Modulation of brain dead induced inflammation by vagus nerve stimulation

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Modulation of brain dead induced inflammation by vagus nerve stimulation.

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