Fig. 1

Brain-systemic crosstalk. After stroke, stimulation of the vagus nerve through nicotinic acetylcholine receptor α7 (nAChRα7) induces microglial activation, causing reduced alveolar macrophage phagocytic capability and reducing circulating levels of interleukin IL-6 and tumour necrosis factor TNF-α, thus leading to an anti-inflammatory reflex and lung injury. On the other hand, systemic inflammation consequent to stroke leads to an increased release of inflammatory mediators such as IL-6 and TNF-α, resulting in lung inflammation and alveolar-capillary injury. Finally, a sympathetic response with increased expression of inflammatory mediators and hypothalamic-pituitary-adrenal axis activation induces elevated glucocorticoid secretion, which might be associated with secondary infections and poor outcome