Peripheral surgery triggers mast cells activation: Focusing on neuroinflammation

Abstract

Peripheral surgery can lead to a systemic aseptic inflammatory response comprising several mediators aiming at restoring tissue homeostasis. It induces inflammatory mechanisms through neuroimmune interaction between the periphery and to brain which also plays a critical role in causing cognitive impairments. Accumulating scientific evidence revealed that acute neuroinflammation of the brain triggered by peripheral surgery that causes peripheral inflammation leads to transmitting signals into the brain through immune cells. Mast cells (MCs) play an important role in the acute neuroinflammation induced by peripheral surgical trauma. After peripheral surgery, brain-resident MCs can be rapidly activated followed by releasing histamine, tryptase, and other inflammatory mediators. These mediators then interact with other immune cells in the peripheral and amplify the signal into the brain by disrupting BBB and activating principle innate immune cells of brain including microglia, astrocytes, and vascular endothelial cells, which release abundant inflammatory mediators and in turn accelerate the activation of brain MCs, amplify the cascade effect of neuroinflammatory response. Surgical stress may induce HPA axis activation by releasing corticotropin-releasing hormone (CRH) subsequently influence the activation of brain MCs, thus resulting in impaired synaptic plasticity. Herein, we discuss the better understating of MCs mediated neuroinflammation mechanisms after peripheral surgery and potential therapeutic targets for controlling inflammatory cascades.

Keywords: Corticotropin-releasing hormone (CRH); Immune cells; Mast cells (MCs); Neuroinflammation; Peripheral surgery.