NF‐κB activation in peripheral blood mononuclear cells in neonatal asphyxia

SUMMARY Neonatal asphyxia results in hypoxic–ischaemic encephalopathy. Previous studies have demonstrated that brain hypoxia and ischaemia lead to the production of proinflammatory cytokines, including tumour necrosis factor‐α (TNF‐α), interleukin‐1 (IL‐1) and IL‐6. Transcription factor NF‐κB is essential for the expression of these cytokines. We examined whether or not NF‐κB is activated in peripheral mononuclear cells (PBMC) in neonatal asphyxia by flow cytometry. In addition, we examined the relationship between NF‐κB activation in PBMC and the neurological prognosis. Flow cytometry analysis demonstrated that the level of NF‐κB activation in CD14+ monocytes/macrophages of the patients with asphyxia who had neurological sequelae was significantly higher than in the controls, and in the patients with asphyxia who survived (31·7 ± 7·2%versus 2·5 ± 0·9%, P = 0·008, and versus 1·6 ± 1·4%, P = 0·014, respectively). Our findings suggest that NF‐κB activation in peripheral blood CD14+ monocytes/macrophages in neonatal asphyxia is important for predicting the subsequent neurological sequelae.