4.5 Article

The vagus nerve alters the pulmonary dendritic cell response to injury

期刊

JOURNAL OF SURGICAL RESEARCH
卷 192, 期 1, 页码 12-18

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2014.06.012

关键词

Burn; Organ/tissue injury; Sepsis/inflammatory response; Acute lung injury; Vagal nerve stimulation

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资金

  1. American College of Surgeons C. James Carrico Faculty Research Fellowship

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Background: We have shown previously that vagal nerve stimulation (VNS) protects against burn-induced acute lung injury (ALI). Although the mobilization and activation of immune cells is central to tissue injury caused by the systemic inflammatory response, the specific inflammatory cell populations that are modulated by VNS have yet to be fully defined. The purpose of this study was to assess whether VNS alters inflammatory cell recruitment to the lung after severe burn injury. Materials and methods: Male C57BL/6 mice were subjected to 30% total body surface area steam burn with and without electrical stimulation of the right cervical vagus nerve. The relative levels of pulmonary dendritic cells (DC) and macrophages were compared at 4 h versus 24 h after burn injury. Lung tissue injury was characterized by histology to assess changes in lung architecture, and measure the protein levels of interleukin 6 and transforming growth factor-beta 1. Results: Severe burn caused an increase in pulmonary DC recruitment at 4 h after injury that persisted at 24 h after severe burn, whereas there was no change in the number of pulmonary macrophages. In contrast, VNS limited the burn-induced recruitment of pulmonary DC. VNS prevented histologic lung injury and attenuated the release of interleukin 6 and transforming growth factor-beta 1 in the lung after burn injury. Conclusions: VNS is an effective method to limit pulmonary DC recruitment to the lung and prevent ALI after burn injury. Identifying strategies to limit inflammatory cell recruitment to the lung may have clinical utility in preventing ALI in severely burned patients. (C) 2014 Elsevier Inc. All rights reserved.

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