Prolonged Loss of Oxidative Phosphorylation and Mitochondrial Mass Characterize CD66b ⁺ Leukocytes from Patients with Sepsis

After sepsis, blood CD66b⁺ cells present with reduced mitochondrial mass and oxidative metabolism that continue at least 6 months after sepsis. These changes in mitochondrial function result from a reduced content of these organelles. We have also identified gene silencing, reduced gene expression of key transcription factors that regulate mitochondrial biogenesis, as well as increased long non-coding RNA as potential drivers of this unique metabolic phenotype. These results highlight the potential benefit of targeting metabolism in sepsis to promote immune homeostasis and recovery.