Hypoxia Induces Histone Clipping and H3K4me3 Loss in Neutrophil Progenitors Resulting in Long-Term Impairment of Neutrophil Immunity

Scientists show that patients three to six months after recovering from acute respiratory distress syndrome have persistently impaired circulating neutrophil effector functions and an increased susceptibility to secondary infections. These defects are linked to a widespread loss of the activating histone mark H3K4me3 in genes that are crucial for neutrophil activities.