Fig. 2

The role of the vagal pathways in the development of lung injury. The healthy brain can control excess cytokine production via an inflammatory reflex of the vagus nerve (by activation of the afferent vagus through the celiac ganglion). Stimulation of the vagus nerve through nicotinic acetylcholine receptor α7 (nAChRα7) regulates microglial activation in the brain, protects neuronal cells from oxidative stress, and improves functional recovery, contributing to immunosuppression. Expression of nAChRα7 on alveolar macrophages and epithelial cells induces a reduction of inflammation in the lungs, and, by suppressing the production of pro-inflammatory cytokines (IL-6, TNF-α) through lipopolysaccharides (LPS) and nuclear factor kappa-light-chain-enhancer of activated B cells (NFK-B), impairs host defence during inflammatory conditions. Altogether, vagal stimulation during stroke blunts macrophage capabilities, with increased risk of infection and lung injury, while paradoxically inducing a higher anti-inflammatory response and thus decreasing the risk of lung injury. The balance between these two pathways accounts for the occurrence, or not, of lung injury. Ach, acetylcholine; NA, noradrenaline