American Journal of Immunology

Effects of Unilateral Cervical Vagotomy on Murine Dendritic Cells

Daniel Sanzio Gimenes da Cruz, Ana Paula Nascimento de Lima, Patrícia Benites Gonçalves da Silva, João Palermo-Neto and Cristina Massoco

DOI : 10.3844/ajisp.2015.48.55

American Journal of Immunology

Volume 11, 2015

Pages 48-55

Abstract

The cholinergic anti-inflammatory pathway has been demonstrated to be an important mechanism that modulates several inflammatory diseases. This modulation occurs upon activation of the vagus nerve, which modulates splenic macrophages and lymphocytes through the predominant neurotransmitter, Acetylcholine (ACh). We hypothesized that this modulation could also take place in dendritic cells, as these cells represent a link between the innate and adaptive immune responses. Bone Marrow-Derived Dendritic Cells (BMDCs) were generated from mice subjected to a unilateral cervical vagotomy and the phenotypes and functions of the BMDCs were evaluated. No significant effects were found in BMDCs from vagotomized mice compared to cells from the control group. The specific immune response was evaluated with the Delayed-Type Hypersensitivity (DTH) skin test using Keyhole Limpet Hemocyanin (KLH) as an antigen and the peak of the response in the vagotomized animals was delayed compared to the control group. It is possible that the Dendritic Cells (DCs) can be modulated by the vagus nerve in other specific sites or under challenging conditions, but our work suggests that immune cells could be modulated by the components of another cholinergic anti-inflammatory pathway or by another neuro-immune pathway interaction.

Copyright

© 2015 Daniel Sanzio Gimenes da Cruz, Ana Paula Nascimento de Lima, Patrícia Benites Gonçalves da Silva, João Palermo-Neto and Cristina Massoco. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.