Inflammatory response is usually associated with various traumatic insults. In addition, traumatic injury produces excessive proinflammatory mediators and subsequent activating or recruiting immune cells into the target organs and results in systemic inflammatory response. However, the complex pathways and mechanisms of inflammatory responses on traumatic injury have not been clearly elucidated. The aim of this special issue is to describe the role of inflammation in traumatic injury, providing an up-to-date viewpoint for therapeutic approaches. Patients after tangential excision surgery usually suffered from tremendous pain, which leads to anxiety, emergency , agitation, and inflammatory reaction. W. Geng et al. showed that preoperative administration of flurbiprofen axetil decreased postoperative tramadol consumption and the visual analog scale after surgery. In addition, flurbiprofen axetil attenuated emergency agitation score and Ramsay score after extubation and reduced the systemic levels of proinflam-matory cytokines tumor necrosis factor-í µí»¼ and interleukin-6 after the operation. The adverse events induced by intubation and extubation may cause intracranial hemorrhage and increase of intracranial pressure, especially in posterior fossa surgery patients. C. Tang et al. suggested that I-gel combined with tracheal intubation could reduce the stress response of posterior fossa surgery patients. Plasma í µí»½-endorphin, corti-sol, interleukin-6, tumor necrosis factor-í µí»¼, malondialdehyde concentrations, and blood glucose were decreased in I-gel facilitated endotracheal tube intubation group. Utilization of I-gel combined with endotracheal tube in posterior fossa surgery may lower inflammatory and oxidative response. Y. Chen et al. reported that sepsis-induced acute intestinal injury was attenuated by dexmedetomidine treatment. The protective effects of dexmedetomidine on sepsis-induced injury may be associated with the inhibition of inflammation via modulating toll-like receptor 4 pathway. Inhalation anesthetics isoflurane may inhibit hypoxia pulmonary vasocon-striction. In addition, dexmedetomidine can reduce the dose of isoflurane inhalation and potentiate hypoxia pulmonary vasoconstriction. R. Xia et al. reported that dexmedeto-midine could augment hypoxia pulmonary vasoconstric-tion and improve oxygenation during one-lung ventilation through inhibiting oxidative stress and increasing nitric oxide release. Histone deacetylases modulate cytokine synthesis and release. Trichostatin A, a histone deacetylase inhibitor, is documented to be anti-inflammatory and neuroprotective. C.-H. Hsing et al. indicated that trichostatin A reduced lipopolysaccharide-induced neuroinflammation and cogni-tive dysfunction. J.-A. Lin et al. first identified the effects of