Editorial: Immune regulation in sepsis

Immune regulation in sepsisSepsis leads to high morbidity and mortality worldwide without effective treatments.Patients with severe sepsis often develop symptoms of persistent inflammation, immunosuppression, and catabolic syndrome involving multiple cell types, organ systems, and pathophysiological mechanisms.Mechanistically, the immune response initiated by an invading pathogen fails to return to normal homeostasis, leading to sustained excessive inflammation and immune suppression in sepsis (1).Sepsis-associated excessive inflammation is prominently featured in leukocytes (i.e., neutrophils, macrophages, natural killer cells), endothelial cells, cytokines, complement products, and the coagulation system, while immunosuppression is related to impaired functions of immune cells (e.g., exhaustion of T cells, apoptosis of T cells, B cells and dendritic cells, reduced human leukocyte antigen-DR isotype (HLA-DR) expression by antigen-presenting cells), diminished production of proinflammatory cytokines through epigenetic modification and increased release of anti-inflammatory cytokines (2).The goal of this Research Topic is to provide a forum to advance research on the contribution of immune system to the development and progression of sepsis.We seek to study the molecular mechanisms of cytokine release syndrome and immunosuppression, develop biomarkers for early diagnosis and prognosis, and explore innovative immunopharmacological interventions to treat sepsis.We have received several original articles that report new targets for curing sepsis.Two of them concerned neutrophil infiltration and function.Ni et al. identified Fpr2 as a negative regulator of Streptococcus suis-induced streptococcal toxic shock-like syndrome (STSLS).They found that Fpr2-knockout mice were less susceptible to STSLS with increased neutrophil recruitment but without an impact on neutrophil extracellular trap (NET) construction.Koutsogiannaki et al. defined aDb2 as a novel potential target of sepsis.They reported that aDb2 deficiency attenuated lung injury and improved survival in experimental polymicrobial abdominal sepsis.Further