Spleen artery embolization aggravates endotoxin hyporesponse of peripheral blood mononuclear cells in patients with spleen injury.

Background: Spleen artery embolization (SAE) increases the success of nonoperative management of spleen injury; however, the immune alternation after SAE is unclear. This study searched the endotoxin responses of peripheral blood mononuclear cells (PBMCs) in injured patients who received SAE. Methods: Patients were subsequently enrolled when their spleen injuries were confirmed by computed tomographic scan. Peripheral blood samples were obtained within first, at third, fifth, and seventh postinjury days. PBMCs were isolated; nuclear factor (NF)-kB translocations, phosphorylated I-kB expressions, and in vitro tumor necrosis factor (TNF)-alpha levels were assayed after endotoxin stimulation (ES). Results: Sixteen patients who received nonoperative managements were enrolled. Five patients received SAE (embolized patients) and 11 patients did not (nonembolized patients). Compared with those in controls, NF-kB translocations, phosphorylated I-kB expressions, and TNF-alpha levels after ES decreased significantly early in injured patients. NF-kB translocation and TNF-alpha levels after ES were indifferent at seventh day between nonembolized patients and controls, whereas significantly lower NF-kB p65 translocation and TNF-alpha levels after ES were found at seventh postinjury day in embolized patients than in controls. Compared with nonembolized patients, embolized patients had significantly lower levels of NF-kBp50 translocations after ES from first to third postinjury days and lower levels of NF-kB p65 translocations, TNF-alpha, and phosphorylated I-kB expressions after ES from first to fifth postinjury days. Conclusions: SAE dysregulates the NF-kB system and aggravates the cytokine hyporesponse upon ES of PBMCs in patients with spleen injury. These results implicate that SAE alters immune response and may increase susceptibility to infections in injured patients.